Method for personalized therapy of celiac disease

Abstract

The present invention relates to a method for selecting or adjusting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one transglutaminase 2 (TG2) inhibitor to said subject, wherein selecting or adjusting the therapy regimen is based on human leukocyte antigen DQ haplotypes of said subject.

Description

Specification The present invention relates to a method for selecting or adjusting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least a treatment of celiac disease by administering a therapeutically effective amount of at least one transglutaminase 2 (TG2) inhibitor to said subject, wherein selecting or adjusting the therapy regimen is based on human leukocyte antigen DQ haplotypes of said subject. Background of the invention Gluten-containing cereals are essential foods worldwide. However, in up to 2% of individuals, the ingestion of dietary gluten results in an abnormal immune response in the small intestine and the development of celiac disease (CeD). Predisposing genotypes, human leukocyte antigen (HLA)-DQ2 and HLA-DQ8, are necessary but not sufficient for the manifestation of CeD. Diarrhea, weight loss, and malnutrition are classical bowel-related symptoms and signs of CeD, but anaemia, osteoporosis, and other autoimmune diseases, such as type 1 diabetes, are also frequent manifestations. Currently, a gluten-free diet (GFD) is the only accepted treatment option for patients with CeD. However, the life-long strict and restrictive GFD is onerous and difficult to follow, and inadvertent gluten ingestion is common, resulting in ongoing symptoms in nearly 50% of treated patients. Keeping the GFD also has a big impact on patients’ quality of life. Inadvertent gluten ingestion often leads to ongoing duodenal mucosal injury, with inflammation and morphological changes. Thus, even patients on GFD frequently have nutrient imbalances and deficiencies. Previous study showed that despite having normal duodenal histomorphology, CeD patients on GFD differ from non-CeD controls on the molecular level and display insufficient expression of micronutrient transporter genes. The CeD autoantigen, transglutaminase 2 (TG2), is expressed in the intestine, where it deamidates certain neutral glutamine residues to negatively charged glutamic acid residues in immunogenic gluten peptides. These modified glutenpeptides are more efficiently presented by HLA-DQ2 or HLA-DQ8 molecules on mucosal antigen-presenting cells, which leads to the activation and expansion of gluten-specific CD4+ type 1 helper T cells and the secretion of pro-inflammatory cytokines. Eventually, this process leads to villus atrophy, crypt hyperplasia, and the production of TG2 IgA. TG2, being crucial for CeD pathogenesis, is a pertinent target for therapy, and this approach was recently tested in a phase 2, randomized, double-blind, placebo-controlled, dose-finding gluten challenge trial using the oral TG2 inhibitor Compound 1. In this phase 2 trial, Compound 1 attenuated gluten-induced duodenal mucosal injury, both morphological deterioration and inflammation, and improved symptoms and quality of life scores in patients with CeD. However, some CeD patients were unexpectedly less responsive to the therapy regimen with Compound 1. Therefore there is a need for a method for selecting or adjusting a therapy regimen for a subject having been diagnosed with celiac disease based on subject’s background, in order to achieve optimal treatment response. It is the objective of the present invention to provide a method for selecting or adjusting a therapy regimen for a subject with celiac disease. The objective of the present invention is solved by the teaching of the independent claims. Further advantageous features, aspects and details of the invention are evident from the dependent claims, the description, the figures, and the examples of the present application. Brief description of the invention Surprisingly, some CeD patients were less responsive to the therapy regimen with Compound 1, suggesting that they could benefit from a longer treatment or higher dosage. The present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one transglutaminase 2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger gluten-specific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures comprising a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applys to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes. Further preferred is a method, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 I HLA-DQ2.2, HLA-DQ2.3 I HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising or consisting of: HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 I DQ2.3, DQ2.5 I DQ2.2, DQ8 I DQ2, DQ2 half heterodimer, DQ2.5 I one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO. Preferred is a computer-implemented method for selecting a therapy regimen, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining an ex-vivo sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said ex-vivo sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. As used herein, the wording “obtaining an ex-vivo sample of genetic material from said subject” does not encompass surgical methods such as the taking of a biopsy. Preferred is a computer-implemented method for selecting a therapy regimen, wherein for a subject applying to the first gluten-sensitive DQ genotype group (i) the therapeutic regimen comprises one or more of administering the TG2 inhibitor at a higher dose, administering the TG2 inhibitor at higher frequency, longer duration of treatment, administering a more potent TG2 inhibitor than a therapeutic regimen for a subject applying to the second gluten-sensitive DQ genotype group (ii) or third gluten-sensitive DQ genotype group (iii). As used herein, the wording “more potent TG2 inhibitor” or “stronger TG2 inhibitor” means that this TG2 inhibitor leads to a better clinical outcome to the therapeutic regimen for a subject applying to the second gluten-sensitive DQ genotype group (ii) or third gluten-sensitive DQ genotype group (iii). Preferred is a computer-implemented method for selecting a therapy regimen, wherein the human leukocyte antigen DQ haplotypes include at least HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 I HLA-DQ2.2, HLA-DQ2.3 I HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising or consisting of: HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 I DQ2.3, DQ2.5 I DQ2.2, DQ8 I DQ2, DQ2 half heterodimer, DQ2.5 I one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO. Preferred is a computer-implemented method for selecting a therapy regimen, wherein step (b) further comprises: identifying said subject as applying to first gluten-sensitive DQ genotype group (i) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.5 I DQ2.5, DQ2.5 I DQ2.3, DQ2.5 / one copy of DQB1*02, or identifying said subject as applying to second gluten-sensitive DQ genotype group (ii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.2 HOMO, DQ8 HOMO, DQ8 / DQ2, DQ2.5 / DQ2.2, or identifying said subject as applying to third gluten-sensitive DQ genotype group (iii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2 half heterodimer, DQ2.2 HETERO, DQ2.5 HETERO, DQ2.5 TrHETERO, DQ8 HETERO, DQ2.5 / one copy of DQA1*05. Preferred is a computer-implemented method for selecting a therapy regimen, wherein a subject applying to the first gluten-sensitive DQ genotype group is characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.7 to -3.0, preferably between -1.0 to -2.7 from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Preferred is a computer-implemented method for selecting a therapy regimen, wherein a subject applying to the second gluten-sensitive DQ genotype group is characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.1 to -1.3, between -0.4 to -1.0 from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Preferred is a computer-implemented method for selecting a therapy regimen, wherein a subject applying to the third gluten-sensitive DQ genotype group is characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.05 to -0.7, preferably between -0.1 to -0.4 from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Preferred is a computer-implemented method for selecting a therapy regimen, wherein the first gluten-sensitive DQ genotype group has a more dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein more dysregulated genexpression is characterized by at least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 (mature enterocytes) are at least 50% more downregulated in the first glutensensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% - 90%; and / or at least one, preferably more than one of the genes AGR2, MKI167, and CENPF (cell proliferation) are at least 30% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 33% - 100%; and / or at least one, preferably more than one of the genes STAT1, GBP1 and TGM2 (inflammation) are at least 50% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% -100%. Preferred is a computer-implemented method for selecting a therapy regimen, wherein the second gluten-sensitive DQ genotype group has a more dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein more dysregulated genexpression is characterized by at least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 (mature enterocytes) are are between 10% - 49% more downregulated in the second gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group; and / or at least one, preferably more than one of the genes AGR2, MKI167, and CENPF (cell proliferation) are between 10% - 29% more upregulated in the second gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 12% - 25%; and / or at least one, preferably more than one of the genes STAT1, GBP1 and TGM2 (inflammation) are between 1% - 49% more upregulated in the second glutensensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 5% - 20%. Preferred is a computer-implemented method for selecting a therapy regimen, wherein the first gluten-sensitive DQ genotype group has a more dysregulated group of (at least two) genes of a biological pathway than the third gluten-sensitive DQ genotype group, wherein a more dysregulated group of (at least two) genes of a biological pathway is characterized by for transit amplifying cells, genes from the first gluten-sensitive DQ genotype group are on average at least 50% more upregulated than genes from the third glutensensitive DQ genotype group, and / or for mature enterocytes genes from the first gluten-sensitive DQ genotype group are on average at least 200% more downregulated than genes from the third gluten-sensitive DQ genotype group; and / or for immune cells, genes from the first gluten-sensitive DQ genotype group are on average at least 100% more upregulated than genes from the third glutensensitive DQ genotype group, and / or for duodenal transporter cells, genes from the first gluten-sensitive DQ genotype group are on average at least 200% more upregulated than genes from the third gluten-sensitive DQ genotype group. Preferred is a computer-implemented method for selecting a therapy regimen, wherein the second gluten-sensitive DQ genotype group has a more dysregulated group of (at least two) genes of a biological pathway than the third gluten-sensitive DQ genotype group, wherein a more dysregulated group of (at least two) genes of a biological pathway is characterized by for transit amplifying cells, genes from the second gluten-sensitive DQ genotype group are on average at least 20% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for mature enterocytes, genes from the second gluten-sensitive DQ genotype group are on average at least 50% more downregulated than genes from the third gluten-sensitive DQ genotype group; and / or for immune cells, genes from the second gluten-sensitive DQ genotype group are on average at least 5% more upregulated than genes from the third glutensensitive DQ genotype group, and / or for duodenal transporter cells, genes from the second gluten-sensitive DQ genotype group are on average at least 50% more upregulated than genes from the third gluten-sensitive DQ genotype group. Preferred is a computer-implemented method for selecting a therapy regimen, wherein step b) further comprises identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as a subject having a risk for refractory coeliac disease or as a subject suffering from refractory coeliac disease; and applying said subject to the first gluten-sensitive DQ genotype group. Preferred is a computer-implemented method for selecting a therapy regimen, wherein the transglutaminase 2 inhibitor is a reversible transglutaminase 2 inhibitor or an irreversible transglutaminase 2 inhibitor. Preferred is a computer-implemented method for selecting a therapy regimen,, wherein the transglutaminase 2 inhibitor is (S,E)-methyl-7-(1 -(2-(2-ethylbutylamino)-2-oxoethyl)-2-oxo-1,2-dihydro-pyridin-3-ylamino)-6-(1 -methyl-1 H-imidazole-5-carboxamido)-7-oxohept-2-enoate (Compound 1): Preferred is a computer-implemented method for selecting a therapy regimen, wherein the therapy regimen comprises at least the use of a pharmaceutical composition comprising the TG2 inhibitor as an active ingredient, together with at least one pharmaceutically acceptable carrier, excipient and / or diluent in the treatment of celiac disease of said subject, preferably wherein the pharmaceutical composition is a systemic formulation. Preferred is a computer-implemented method for selecting a therapy regimen, wherein the TG2 inhibitor is a reversible TG2 inhibitor or an irreversible TG2 inhibitor. Preferred is a method for for selecting a therapy regimen, wherein the transglutaminase 2 inhibitor is administered to the subject as pharmaceutical composition comprising the TG2 inhibitor as an active ingredient, together with at least one pharmaceutically acceptable carrier, excipient and / or diluent, preferably wherein the pharmaceutical composition is a systemic formulation, preferably an oral formulation. Description of the invention Definitions Currently used predictive markers of therapy for celiac disease: a) Attenuation of gluten-induced small intestinal mucosal injury as measured by the VH:CrD ratio. The VH:CrD is the morphometric measure of the length of the small intestinal villi with respect to the depth of the crypts taken from an intestinal biopsy sample. (b) Attenuation of gluten-induced small intestinal mucosal inflammation as measured by the enumeration of intraepithelial lymphocytes (lELs) in histological sections. (c) Attenuation of gluten-induced serum antibodies such as anti-gliadin antibodies and autoantibodies against transglutaminase. The term “celiac disease” or “CD”, as used herein, refers to a disorder of the intestinal mucosa that is typically associated with villous atrophy, crypt hyperplasia, and / or inflammation of the mucosal lining of the small intestine. In addition to the malabsorption of nutrients, individuals with celiac disease are at risk for mineral deficiency, vitamin deficiency, osteoporosis, autoimmune diseases, and intestinal malignancies, such as lymphoma and carcinoma. It is thought that celiac disease is mostly caused by exposure to proteins such as gluten, e.g., glutenin and prolamine proteins which are present in wheat, rye, barley, oats, millet, triticale, spelt, and kamut, in the appropriate genetic and environmental context. The term “refractory celiac disease” or “refractory CD”, as used herein, refers to a rare intestinal disorder characterized by persistent or recurrent symptoms and signs of confirmed celiac disease despite a long-term, strict gluten-free diet, without other causes of villous atrophy or malignant complications, and with or without the presence of increased abnormal intraepitelial lymphocytes. Refractory celiac disease (RCD) is a complex autoimmune disorder much like the more common celiac disease but, unlike celiac disease, it is resistant or unresponsive to at least 6-12 months of treatment with a strict gluten-free diet. In celiac disease, treatment by means of a strict gluten-free diet is usually sufficient to overcome the disorder. However, refractory celiac disease is just that: refractory or stubbornly resistant to treatment. Only a small percentage (1-2%) of the people with celiac disease will develop RCD. The term “sample” or “biological sample”, as used herein, includes a biological specimen obtained from a subject. Suitable samples for use in the present invention include, without limitation, whole blood, plasma, serum, saliva, urine, stool (feces), tears, any other bodily fluid, tissue samples (e.g., biopsy), and cellular extracts thereof, e.g. red blood cellular extract. A preferred sample is a whole blood sample or a serum sample. The use of samples such as serum, saliva, and urine and isolation of nucleic acids from such samples + prior to HLA-DQ genotyping is well known in the art. As used herein, the wording “obtaining an ex-vivo sample of genetic material from said subject” does not encompass surgical methods such as the taking of a biopsy. Thus, suitable samples for use in the present invention include, without limitation, ex-vivo samples selected from whole blood, plasma, serum, saliva, urine, stool (feces), tears, any other bodily fluid, tissue samples, and cellular extracts thereof, e.g. red blood cellular extract. A preferred ex-vivo sample is a whole blood sample or a serum sample. The term "subject", as used herein, refers to an individual or patient having been diagnosed with celiac disease, preferably having a risk of refractory celiac disease or having been diagnosed with refractory celiac disease. The subject may be already in treatment of celiac disease or refractory celiac disease, e.g. may receive a therapeutically effective amount of at least one transglutaminase 2 inhibitor to said subject, preferably a therapeutically effective amount of Compound 1 or may receive a pharmaceutical composition comprising a therapeutically effective amount of Compound 1. A subject may be herein also an individual with well-controlled celiac disease who participated in the phase Ila, double-blind, randomised, placebo-controlled, dose-finding study on the efficacy and tolerability of a 6-week treatment with Compound 1 capsules vs. placebo in subjects undergoing gluten challenge. However, such a subject who participated in the phase Ila, double-blind, randomised, placebo-controlled, dose-finding study on the efficacy and tolerability of a 6-week treatment with Compound 1 capsules vs. placebo in subjects undergoing gluten challenge herein may be preferably herein used as a comparative subject. The term “human leukocyte antigen class II” or “HLA Class II”, as used herein, refers to a group of genes in the human leukocyte antigen (HLA) system, located within the Major Histocompatibility Complex (MHC) on chromosome 6. These genes encode for proteins that are expressed on the surface of antigen-presenting cells such as dendritic cells, B cells, and macrophages and crucial for the immune system's ability to recognize and present antigens. The term "human leukocyte antigen (HLA) class II genotype", as used herein, refers to the specific combination of alleles (versions of a gene) at the HLA class II loci on chromosome 6 in an individual's genome. The term “haplotype”, as used herein, refers to a group of genes that are located close to each other on the same chromosome within an organism and usually inherited together from a single parent. The term "allele", as used herein, refers to one of two or more versions of a gene that are found at the same place, or locus, on a chromosome. The term “dysregulated gene expression”, as used herein, refers to gluten-induced transcriptomic changes (dependent on the gene, higher or lower RNA level) measurable for patients suffering from celiac disease when challenged with gluten. Gluten-induced transcriptomic changes can preferably be determined by RNA-sequencing analysis of RNA extracts derived from patients suffering from celiac disease. In contrary, gluten-induced transcriptomic changes are not observed in healthy subjects, e.g. subjects that are not suffering from celiac disease. Moreover, for patients suffering from celiac disease on gluten-free diet also no gluten-induced transcriptomic changes should be observable. Thus, the basic transcriptomic level would be e.g. a transcriptomic profile of either healthy subject or patients not challenged with gluten. It has been surprisingly found that the human leukocyte antigen DQ haplotypes of a subject have an impact on the severity of gluten-induced transcriptomic changes for a subject. According to the invention, based on the human leukocyte antigen DQ haplotypes of a subject, a subject can be assigned to one of three glutensensitive DQ genotype groups. It has been found the gene expression, i.e. the gluten-induced transcriptomic changes is more dysregulated for subjects applying to the first gluten-sensitive group than for subjects applying to the second or third gluten-sensitive group, and that the gene expression, i.e. the gluten-induced transcriptomic changes is more dysregulated for subjects applying to the second gluten-sensitive group than for subjects applying to the third gluten-sensitive group. Thus, “more dysregulated gene expression” means that more gluten-induced transcriptomic changes (dependent on the gene, higher or lower RNA level) are observed when comparing DQ genotype group (i) (first gluten-sensitive DQ genotype group) with DQ genotype group (ii) (second gluten-sensitive DQ genotype group), and / or when comparing DQ genotype group (ii) (second glutensensitive DQ genotype group) with DQ genotype group (iii) (third gluten-sensitive DQ genotype group). Moreover, “more dysregulated gene expression” preferably means that genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation are more up and / or downregulated for patients of DQ genotype group (i) (first gluten-sensitive DQ genotype group) than for patients of DQ genotype group (ii) and (iii) (second and third gluten-sensitive DQ genotype group). Furthermore, “more dysregulated gene expression” preferably means that genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation are more up and / or downregulated for patients of DQ genotype group (ii) (second gluten-sensitive DQ genotype group) than for patients of DQ genotype group (iii) (second and third gluten-sensitive DQ genotype group). Thus, preferably the first gluten-sensitive DQ genotype group has a more dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein more dysregulated genexpression is characterized by at least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 (mature enterocytes) are at least 50% more downregulated in the first glutensensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% - 90%; and / or at least one, preferably more than one of the genes AGR2, MKI167, and CENPF (cell proliferation) are at least 30% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 33% - 100%; and / or at least one, preferably more than one of the genes STAT1, GBP1 and TGM2 (inflammation) are at least 50% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% -100%. Thus, preferably the second gluten-sensitive DQ genotype group has a more dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein more dysregulated genexpression is characterized by at least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 (mature enterocytes) are are between 10% - 49% more downregulated in the second gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group; and / or at least one, preferably more than one of the genes AGR2, MKI167, and CENPF (cell proliferation) are between 10% - 29% more upregulated in the second gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 12% - 25%; and / or at least one, preferably more than one of the genes STAT1, GBP1 and TGM2 (inflammation) are between 1% - 49% more upregulated in the second glutensensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 5% - 20%. Moreover, preferably the first gluten-sensitive DQ genotype group has a more dysregulated group of (at least two) genes of a biological pathway than the third gluten-sensitive DQ genotype group, wherein a more dysregulated group of (at least two) genes of a biological pathway is characterized by for transit amplifying cells, genes from the first gluten-sensitive DQ genotype group are on average at least 50% more upregulated than genes from the third glutensensitive DQ genotype group, and / or for mature enterocytes genes from the first gluten-sensitive DQ genotype group are on average at least 200% more downregulated than genes from the third gluten-sensitive DQ genotype group; and / or for immune cells, genes from the first gluten-sensitive DQ genotype group are on average at least 100% more upregulated than genes from the third glutensensitive DQ genotype group, and / or for duodenal transporter cells, genes from the first gluten-sensitive DQ genotype group are on average at least 200% more upregulated than genes from the third gluten-sensitive DQ genotype group. Moreover, preferably the second gluten-sensitive DQ genotype group has a more dysregulated group of (at least two) genes of a biological pathway than the third gluten-sensitive DQ genotype group, wherein a more dysregulated group of (at least two) genes of a biological pathway is characterized by for transit amplifying cells, genes from the second gluten-sensitive DQ genotype group are on average at least 20% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for mature enterocytes, genes from the second gluten-sensitive DQ genotype group are on average at least 50% more downregulated than genes from the third gluten-sensitive DQ genotype group; and / or for immune cells, genes from the second gluten-sensitive DQ genotype group are on average at least 5% more upregulated than genes from the third glutensensitive DQ genotype group, and / or for duodenal transporter cells, genes from the second gluten-sensitive DQ genotype group are on average at least 50% more upregulated than genes from the third gluten-sensitive DQ genotype group. The term “first gluten-sensitive DQ genotype group” or “high gluten-sensitive group”, as used herein, refers to the group of patients (i.e. subjects) who exhibit a robust gluten-specific T-cell response when exposed to gluten. This immune reaction leads to a decrease in the villous height to crypt depth (VH:CrD) ratio and a marked epithelial response to interferon-gamma (IFNy) during a six-week gluten challenge. Preferably, the patients (i.e. subjects) of the “first gluten-sensitive group” are characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.7 to -3.0 (-0.7 > VH:CrD ratio > -3.0), particularly preferably between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from GFD. The VH:CrD ratio of the first or high gluten-sensitive group is lower than the VH:CrD ratio of the second or mid gluten-sensitive group. Thus, a subject applying to the “first gluten-sensitive DQ genotype group” is characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.7 to -3.0 (-0.7 > VH:CrD ratio > -3.0), preferably between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Moreover, a subject applying to the first gluten-sensitive DQ genotype group receiving a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of celiac disease is preferably also characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.41 to -0.60 (-0.41 > VH:CrD ratio > -0.60) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. As a reference value for the ratio villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet a VH:CrD value of about 2.00, a VH:CrD value range between 2.00 - 2.20, or a VH:CrD value 2.11 ±0.34 may applied. The comparative subject on gluten-free diet may be also the subject in case the VH:CrD value of the subject on gluten-free diet is available. The term “second gluten-sensitive DQ genotype group” or “mid glutensensitive group”, as used herein, describes patients (i.e. subjects) who demonstrate a moderate gluten-specific T-cell response after being exposed to gluten. This immune response leads to alterations in the villous height to crypt depth (VH:CrD) ratio and an epithelial response to interferon-gamma (IFNy) during a six-week gluten challenge, with the seventy of these changes falling between those observed in high and low gluten-sensitive individuals. Preferably, the patients (i.e. subjects) of the “second gluten-sensitive group” are characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.1 to -1.3 (-0.1 > VH:CrD ratio > -1.3), particularly preferably between -0.4 to -1.0 (-0.4 > VH:CrD ratio > -1.0) from GFD. The VH:CrD ratio of the second or mid gluten-sensitive group is lower than the VH:CrD ratio of the third or low glutensensitive group. Thus, a subject applying to the second gluten-sensitive DQ genotype group is characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.1 to -1.3 (-0.1 > VH:CrD ratio > -1.3), between -0.4 to -1.0 (-0.4 > VH:CrD ratio > -1.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Moreover, a subject applying to the second gluten-sensitive DQ genotype group receiving a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of celiac disease is preferably also characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.16 to -0.40 (-0.16 > VH:CrD ratio > -0.40) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. As a reference value for the ratio villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet a VH:CrD value of about 2.00, a VH:CrD value range between 2.00 - 2.20, or a VH:CrD value 2.11 ±0.34 may applied. The comparative subject on gluten-free diet may be also the subject in case the VH:CrD value of the subject on gluten-free diet is available. The term “third gluten-sensitive DQ genotype group” or “low gluten-sensitive group”, as used herein, refers to the group of patients (i.e. subjects) who exhibit a minimal gluten-specific T-cell response upon gluten exposure. Such immune reaction results in the maintenance of the villous height to crypt depth (VH:CrD) ratio and negligible epithelial response to interferon-gamma (IFNy) throughout a six-week gluten challenge. Preferably, the patients (i.e. subjects) of the “third gluten-sensitive group” are characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.05 to -0.7 (-0.05 > VH:CrD ratio > -0.7), particularly preferably between -0.1 to -0.4 (-0.1 > VH:CrD ratio > -0.4) from GFD. Thus, a subject applying to the third gluten-sensitive DQ genotype group is characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.05 to -0.7 (-0.05 > VH:CrD ratio > -0.7), preferably between -0.1 to -0.4 (-0.1 > VH:CrD ratio > -0.4) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Moreover, a subject applying to the third gluten-sensitive DQ genotype group receiving a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of celiac disease is preferably also characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.05 to -0.15 (-0.05 > VH:CrD ratio > -0.15) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. As a reference value for the ratio villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet a VH:CrD value of about 2.00, a VH:CrD value range between 2.00 - 2.20, or a VH:CrD value 2.11 ±0.34 may applied. The comparative subject on gluten-free diet may be also the subject in case the VH:CrD value of the subject on gluten-free diet is available. As used herein, a “pharmaceutically effective amount” of a transglutaminase 2 inhibitor is the amount or activity effective for achieving the desired physiological result, either in cells treated in vitro or in a patient treated in vivo. Specifically, a pharmaceutical effective amount is such an amount which is sufficient for inhibiting, for a certain period of time, one or more of the clinically defined pathological processes associated with transglutaminase 2. The effective amount can vary according to the specific compound of the formula (I) and additionally depends on a plurality of factors and conditions related to the subject to be treated and the severity of the disease. If, for example, an inhibitor is to be administered in vivo, factors such as age, weight and health of the patients as well as dose reaction curves and data regarding toxicity obtained from preclinical animal studies are amongst the data to be considered. If the inhibitor in form of the compound of the formula (I) described herein is to be brought in contact with the cells in vivo, a plurality of preclinical in vitro studies would be designed in order to determine parameters such as absorption, half-life, dose, toxicity, etc.. Determining a pharmaceutically effective amount for a given pharmaceutically active ingredient is part of the ordinary skills of the one skilled in the art. The term “more potent TG2 inhibitor” or “stronger TG2 inhibitor”, as used herein, refers to a TG2 inhibitor with a lower half maximal inhibitory concerntration (IC50) when compared to a different TG-2 inhibitor. For instance, treatment of patients of the DQ genotype group (i) (first gluten-sensitive DQ genotype group) can be treated with TG2 inhibitor A (e.g. Compound 1) and patients of the DQ genotype group (ii) (second gluten-sensitive DQ genotype group) can be / are treated with TG2 inhibitor B (e.g. a different TG2 inhibitor than Compound 1 as disclosed herein), whereby TG2 inhibitor A (e.g. Compound 1) has lower IC50 than TG2 inhibitor B (e.g. a different TG2 inhibitor than Compound 1 as disclosed herein). Method for selecting a therapeutic regimen The efficacy of the TG2 inhibitor Compound 1 to attenuate gluten-induced mucosal damage was previously reported in a proof-of-concept, randomized, double-blind, placebo-controlled, 6-week trial with a daily 3-g gluten challenge. TG2, the celiac autoantigen, has a pivotal role in gluten-induced pathogenesis, leading to small intestinal mucosal injury, with villus atrophy and crypt hyperplasia, the histological hallmarks of untreated CeD. Here, the inventors sought to assess the efficacy of Compound 1 in preventing gluten-induced mucosal damage at the transcriptomic level (Example 1). Remarkably, a 100 mg daily dose of Compound 1 inhibited virtually all the gluten-induced transcriptomic changes (Figure 1B, C). Active CeD is accompanied by compromised enterocyte maturation, crypt hyperplasia due to the expansion of transit amplifying cells, immune cell infiltration, and decreased expression of duodenal transporters. GSZ scores based on published single-cell databases clearly indicated that TG2 inhibition efficiently blocked all the aforementioned gluten-induced intestinal manifestations in patients with CeD (Figure 2D). A recently published molecular histomorphometry regression model based on genome-wide transcriptomics analysis was validated in the independent study sample (Example 1). The inventors showed a significant accordance between this new molecular tool and the traditional, more subjective biopsy-based microscopic histomorphometry reading. Overall, the transcriptomic findings strongly support the results of the clinical trial with Compound 1, which demonstrated that the inhibition of TG2 activity can efficiently and specifically prevent gluten-induced mucosal damage. In addition, studies have shown that gluten-derived peptides may have innate immune stimulatory properties, outside the realm of adaptive immunity, which can lead to epithelial stress in CeD. The inventors’ data shows, however, that halting the adaptive immunity pathway in CeD pathogenesis is sufficient to prevent gluten-induced mucosal damage as the inventors did not detect any molecular traces of mucosal damage remaining after the Compound 1 treatment. Gene ontology and reactome analyses indicated that gluten challenge most significantly affected genes related to the immune response, and especially to interferon-mediated defense mechanisms (Figure 2B and 2C). This is in accordance with previously published transcriptomic analyses of active CeD patients compared to patients on GFD or healthy controls. Notably, IFN-y secreted by gluten-reactive T cells in the celiac intestine induces TG2 expression and secretion, and thus favors the pathogenic auto-amplificatory loop of enhanced gluten deamidation by TG2, improved antigenic presentation on HLA-DQ2 or -DQ8, and subsequent gluten-specific T cell activation. The study as described in Example 1 confirms the prominent role of interferon signaling in CeD pathogenesis, in line with findings that nearly half of the gluten-induced gene expression changes in duodenal biopsies can be recapitulated in human intestinal epithelial organoids treated with IFN-y (Figure 3A). The inventors also detected the suggested auto-amplificatory loop in the patient data, as TG2 expression positively correlated with the epithelial IFN-y response (Figure 3F). Notably, TG2 expression was induced by IFN-y in human intestinal organoids ex vivo (Figure 3E), suggesting mutual amplification between these two key players in CeD pathogenesis. The functional relevance of this amplification loop was indeed confirmed in the clinical study in which the inhibition of TG2 activity by Compound 1 in patients with CeD significantly inhibited both the (epithelial) IFN-y response (Figure 3B) and TG2 expression (Figure 3C), resulting in protection from villous atrophy and intraepithelial lymphocytosis (Figure 2D). However, even though TG2 inhibition exhibited significant efficacy, according to a comparison of the transcripts of the placebo / gluten challenge and the gluten challenge / Compound 1-treated group, which showed a transcriptome profile similar to the GFD groups, the inventors detected heterogeneity regarding the gluten-induced and IFN-y-dependent cascade of pathogenic events among the Compound 1-treated and gluten-challenged CeD patients. Four of these patients still had a modestly active IFN-y response, and the majority (three out of four) belonged to the HLA-DQ2.5 homozygous genotype (Figure 3C) (Example 2). HLA-DQ2.5 homozygous individuals have a fivefold higher risk of developing CeD compared to HLA-DQ2.5 heterozygous individuals, which has been linked to the more efficient presentation of deamidated gluten peptides to gluten-specific T cells. Moreover, homozygosity for HLA-DQ2 predisposes patients to developing more rapid and severe villous atrophy and is associatedwith malignant complications such as refractory CeD type II (RCD II) and enteropathy-associated T-cell lymphoma (EATL). Along this line, the inventors also found that patients belonging to the high gluten-response DQ genotype group (G1) were more sensitive to gluten, as their VH:CrD dropped significantly more compared to patients belonging to the mid- and low-gluten response groups (G2 and G3) during the gluten challenge, both in the placebo and drug groups (Tables 4 and 6 and Figure 4A and 4B). Thus, even after drug treatment, VH:CrD decreased significantly in the G1 versus G2 and G3 genotype groups after the gluten challenge. This was also evident when molecular histomorphometric features were assessed (Figure 9C and 9D). The inventors also have found that PPAR signaling and lipid metabolism, previously reported to be dysregulated in CeD, were less controlled in G1 group (Figure 9C and 9D). As IFN-y is known to inhibit PPAR and lipid metabolism, it is conceivable that these are consequent of the overactive IFN-y response in G1 group patients. Nevertheless, duodenal mucosal morphology and, especially, intraepithelial lymphocyte infiltration were significantly healthier in the Compound 1-treated group compared to the placebo group, indicating that patients with G1 phenotypes may benefit from a higher dose and / or prolonged treatment with Compound 1. The inventors suggest that the Compound 1 therapy program should include a personalized medicine approach in which HLA-DQ stratification with TG2-inhibitor dose adjusted accordingly may lead to an optimal treatment response and a more thorough abrogation of the IFN-y-induced mucosal damage. According to the transcriptomic analysis of human intestinal organoids, Compound 1 does not appear to induce significant transcriptomic changes in the organoid model (Figure 6), consistent with the clinical safety observed in the phase 2 challenge study. In conclusion, the strategy to inhibit TG2 activity as a key upstream effector in gluten-induced immune activation in CeD, which has been proven efficient in the clinical study, was mechanistically buttressed by the inventors’ transcriptomic analysis of the duodenal biopsies of patients treated or untreated with Compound 1. Importantly, TG2 inhibition prominently prevented the gluten-induced IFN-y response and further downstream pathways that led to mucosal inflammation, remodeling, and villous atrophy. The inventors analysis also suggested that based on the HLA-DQ 2.5 genetics, the dose or dose interval of Compound 1 should be adjusted for optimal efficacy. Moreover, CeD-associated gene expression changes were observable, even on a strict GFD indicating that complete avoidance of gluten is impossible. In fact, a recent meta-analysis found that 15% of foods labeled as gluten-free and 28% labeled as naturally gluten-free contained more than 20 mg / kg of gluten, the cut-off for qualifying as gluten-free. Thus, an adjunctive TG2 inhibition-based therapy accompanied with the GFD would especially benefit patients belonging to a highly gluten-sensitive group, possibly carrying a homozygous HLA-DQ genotype by providing protection against intestinal damage that can occur even in a low gluten environment. Embodiments for Method for selecting a therapeutic regimen The present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures comprising a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, and preferably wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising or consisting of: HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO. Preferred is a computer-implemented method for selecting a therapy regimen, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining an ex-vivo sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said ex-vivo sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. In all embodiment of the present invention, the therapy regimen preferably comprises TG2 inhibitor at a daily dose between 0.1 mg - 1000 mg, preferably between 0.5 mg - 500 mg, more preferably between 0.75 mg - 250 mg, most preferably between 1 mg - 100 mg. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose between 150 mg - 250 mg, more preferably between 160 mg - 240 mg, more preferably between 170 mg - 230 mg, more preferably between 180 mg - 220 mg, more preferably between 190 mg - 210 mg. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose of (about) 200 mg. More preferably, in all embodiments of the present invention, therapy regimen for the first gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 25 mg - 1000 mg, preferably between 25 mg - 500 mg, more preferably between 25 mg - 250 mg, most preferably between 30 mg - 100 mg, and / or wherein the therapy regimen for the second gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 5 mg - 750 mg, more preferably between 5 mg - 250 mg, preferably between 5 mg - 75 mg, most preferably between 10 mg - 30 mg, and / or wherein the therapy regimen for the third gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 0.1 mg - 500 mg, more preferably between 0.1 mg - 250 mg, preferably between 0.1 mg - 50 mg, most preferably between 1 mg - 10 mg. In some preferred embodiments, the therapy regimen regimen for the first glutensensitive DQ genotype group preferably comprises TG2 inhibitor at a daily dose between 150 mg - 250 mg, more preferably between 160 mg - 240 mg, more preferably between 170 mg - 230 mg, more preferably between 180 mg - 220 mg, more preferably between 190 mg - 210 mg. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose of (about) 200 mg. In preferred embodiments of the present invention, the therapy regimen for the first gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 25 mg - 1000 mg, and / or wherein the therapy regimen for the second gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 5 mg - 750 mg, and / or wherein the therapy regimen for the third gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 0.1 mg - 500 mg. In further preferred embodiments of the present invention, the therapy regimen for the first gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 25 mg - 500 mg, and / or wherein the therapy regimen for the second gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 5 mg - 250 mg, and / or wherein the therapy regimen for the third gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 0.1 mg - 250 mg. In even further preferred embodiments of the present invention, the therapy regimen for the first gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 25 mg - 250 mg, and / or wherein the therapy regimen for the second gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 5 mg - 75 mg, and / or wherein the therapy regimen for the third gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 0.1 mg - 50 mg. In even further preferred embodiments of the present invention, the therapy regimen for the first gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 150 mg - 250 mg, more preferably between 160 mg - 240 mg, more preferably between 170 mg - 230 mg, more preferably between 180 mg - 220 mg, more preferably between 190 mg - 210 mg, most preferably of (about) 200 mg, and / or wherein the therapy regimen for the second gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 5 mg - 75 mg, and / or wherein the therapy regimen for the third gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 0.1 mg - 50 mg. In some further preferred embodiments of the present invention, the therapy regimen for the first gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 30 mg - 100 mg, and / or wherein the therapy regimen for the second gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 10 mg - 30 mg, and / or wherein the therapy regimen for the third gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 1 mg - 10 mg. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, and preferably wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising or consisting of: HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO, wherein for a subject applying to the first gluten-sensitive DQ genotype group (i) the therapeutic regimen comprises one or more of administering the TG2 inhibitor at a higher dose, administering the TG2 inhibitor at higher frequency, longer duration of treatment, administering a more potent TG2 inhibitor than a therapeutic regimen for a subject applying to the mid gluten-sensitive DQ genotype group (ii) or low gluten-sensitive DQ genotype group (iii). A more potent TG2 inhibitor refers to a TG2 inhibitor with a lower half maximal inhibitory concerntration (IC50) when compared to a different TG-2 inhibitor. For instance, treatment of patients of the DQ genotype group (i) (first gluten-sensitive DQ genotype group) can be treated with Compound 1 and patients of the DQ genotype group (ii) or (iii) (second gluten-sensitive DQ genotype group) can be treated with a different TG2 inhibitor as disclosed herein, whereby Compound 1 has lower IC50 than the other TG2 inhibitor as disclosed herein. Preferred is a computer-implemented method for selecting a therapy regimen, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining an ex-vivo sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said ex-vivo sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger gluten specific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, at least HLA-DQ2 and HLA-DQ8 haplotypes, an preferably wherein the HLA-DQ2 haplotypes are selected from the group consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group consisting of: HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO. Preferred is a computer-implemented method for selecting a therapy regimen, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining an ex-vivo sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said ex-vivo sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein for a subject applying to the first gluten-sensitive DQ genotype group (i) the therapeutic regimen comprises one or more of administering the TG2 inhibitor at a higher dose, administering the TG2 inhibitor at higher frequency, longer duration of treatment, administering a more potent TG2 inhibitor than a therapeutic regimen for a subject applying to the second gluten-sensitive DQ genotype group (ii) or third gluten-sensitive DQ genotype group (iii), wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, at least HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group consisting of: HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO. Preferred is a computer-implemented method for selecting a therapy regimen, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining an ex-vivo sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said ex-vivo sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising of consisting of: HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO; wherein step (b) further comprises: identifying said subject as applying to first gluten-sensitive DQ genotype group (i) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.5 I DQ2.5, DQ2.5 I DQ2.3, DQ2.5 / one copy of DQB1*02, or identifying said subject as applying to second gluten-sensitive DQ genotype group (ii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.2 HOMO, DQ8 HOMO, DQ8 / DQ2, DQ2.5 / DQ2.2, or identifying said subject as applying to third gluten-sensitive DQ genotype group (iii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2 half heterodimer, DQ2.2 HETERO, DQ2.5 HETERO, DQ2.5 TrHETERO, DQ8 HETERO, DQ2.5 / one copy of DQA1*05. Preferred is a computer-implemented method for selecting a therapy regimen, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining an ex-vivo sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said ex-vivo sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, the therapy regimen preferably comprises TG2 inhibitor at a daily dose between 0.1 mg - 1000 mg, preferably between 0.5 mg - 500 mg, more preferably between 0.75 mg - 250 mg, most preferably between 1 mg - 100 mg. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose between 150 mg - 250 mg, more preferably between 160 mg - 240 mg, more preferably between 170 mg - 230 mg, more preferably between 180 mg - 220 mg, more preferably between 190 mg - 210 mg. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose of (about) 200 mg. More preferably, the therapy regimen for the first gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 25 mg - 1000 mg, preferably between 25 mg - 500 mg, more preferably between 25 mg - 250 mg, most preferably between 30 mg - 100 mg, and / or wherein the therapy regimen for the second gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 5 mg - 750 mg, more preferably between 5 mg - 250 mg, preferably between 5 mg - 75 mg, most preferably between 10 mg - 30 mg, and / or wherein the therapy regimen for the third gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 0.1 mg - 500 mg, more preferably between 0.1 mg - 250 mg, preferably between 0.1 mg - 50 mg, most preferably between 1 mg - 10 mg. In some preferred embodiments, the therapy regimen regimen for the first glutensensitive DQ genotype group preferably comprises TG2 inhibitor at a daily dose between 150 mg - 250 mg, more preferably between 160 mg - 240 mg, more preferably between 170 mg - 230 mg, more preferably between 180 mg - 220 mg, more preferably between 190 mg - 210 mg. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose of (about) 200 mg. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein for a subject applying to the first gluten-sensitive DQ genotype group (i) the therapeutic regimen comprises one or more of administering the TG2 inhibitor at a higher dose, administering the TG2 inhibitor at higher frequency, longer duration of treatment, administering a stronger TG2 inhibitor than a therapeutic regimen for a subject applying to the mid gluten-sensitive DQ genotype group (ii) or low gluten-sensitive DQ genotype group (iii), wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, at least HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group consisting of: HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO; wherein step (b) further comprises: identifying said subject as applying to first gluten-sensitive DQ genotype group (i) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.5 I DQ2.5, DQ2.5 I DQ2.3, DQ2.5 / one copy of DQB1*02, or identifying said subject as applying to second gluten-sensitive DQ genotype group (ii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.2 HOMO, DQ8 HOMO, DQ8 / DQ2, DQ2.5 / DQ2.2, or identifying said subject as applying to third gluten-sensitive DQ genotype group (iii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2 half heterodimer, DQ2.2 HETERO, DQ2.5 HETERO, DQ2.5 TrHETERO, DQ8 HETERO, DQ2.5 / one copy of DQA1*05. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein for a subject applying to the first gluten-sensitive DQ genotype group (i) the therapeutic regimen comprises one or more of administering the TG2 inhibitor at a higher dose, administering the TG2 inhibitor at higher frequency, longer duration of treatment, administering a more potent TG2 inhibitor than a therapeutic regimen for a subject applying to the second gluten-sensitive DQ genotype group (ii) or third gluten-sensitive DQ genotype group (iii), wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising or consisting of: HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO, wherein step (b) further comprises: identifying said subject as applying to first gluten-sensitive DQ genotype group (i) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.5 I DQ2.5, DQ2.5 I DQ2.3, DQ2.5 / one copy of DQB1*02, or identifying said subject as applying to second gluten-sensitive DQ genotype group (ii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.2 HOMO, DQ8 HOMO, DQ8 / DQ2, DQ2.5 / DQ2.2, or identifying said subject as applying to third gluten-sensitive DQ genotype group (iii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2 half heterodimer, DQ2.2 HETERO, DQ2.5 HETERO, DQ2.5 TrHETERO, DQ8 HETERO, DQ2.5 / one copy of DQA1*05. Preferred is a computer-implemented method for selecting a therapy regimen, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining an ex-vivo sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said ex-vivo sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising or consisting of: HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO, wherein the TG2 inhibitor is a reversible TG2 inhibitor or an irreversible TG2 inhibitor. In particular preferred embodiments, the transglutaminase 2 inhibitor is (S,E)-methyl-7-(1-(2-(2-ethylbutylamino)-2-oxoethyl)-2-oxo-1,2-dihydro-pyridin-3-yl-amino)-6-(1-methyl-1 H-imidazole-5-carboxamido)-7-oxohept-2-enoate (Compound 1). Preferred is a computer-implemented method for selecting a therapy regimen, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining an ex-vivo sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said ex-vivo sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising or consisting of: HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 I one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO, wherein step (b) further comprises: identifying said subject as applying to first gluten-sensitive DQ genotype group (i) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.5 I DQ2.5, DQ2.5 I DQ2.3, DQ2.5 / one copy of DQB1*02, or identifying said subject as applying to second gluten-sensitive DQ genotype group (ii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.2 HOMO, DQ8 HOMO, DQ8 / DQ2, DQ2.5 / DQ2.2, or identifying said subject as applying to third gluten-sensitive DQ genotype group (iii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2 half heterodimer, DQ2.2 HETERO, DQ2.5 HETERO, DQ2.5 TrHETERO, DQ8 HETERO, DQ2.5 / one copy of DQA1*05, wherein the TG2 inhibitor is a reversible TG2 inhibitor or an irreversible TG2 inhibitor. In particular preferred embodiments, the transglutaminase 2 inhibitor is (S,E)-methyl-7-(1-(2-(2-ethylbutylamino)-2-oxoethyl)-2-oxo-1,2-dihydro-pyridin-3-ylamino)-6-(1-methyl-1 H-imidazole-5-carboxamido)-7-oxohept-2-enoate (Compound 1). Preferred is a computer-implemented method for selecting a therapy regimen, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining an ex-vivo sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said ex-vivo sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, the present invention relates to a method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein for a subject applying to the first gluten-sensitive DQ genotype group (i) the therapeutic regimen comprises one or more of administering the TG2 inhibitor at a higher dose, administering the TG2 inhibitor at higher frequency, longer duration of treatment, administering amore potent TG2 inhibitor than a therapeutic regimen for a subject applying to the second gluten-sensitive DQ genotype group (ii) or third gluten-sensitive DQ genotype group (iii), wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising or consisting of: HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO; wherein the TG2 inhibitor is a reversible TG2 inhibitor or an irreversible TG2 inhibitor. In particular preferred embodiments, the transglutaminase 2 inhibitor is (S,E)-methyl-7-(1-(2-(2-ethylbutylamino)-2-oxoethyl)-2-oxo-1,2-dihydro-pyridin-3-ylamino)-6-(1-methyl-1 H-imidazole-5-carboxamido)-7-oxohept-2-enoate (Compound 1). Preferred is a computer-implemented method for selecting a therapy regimen, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining an ex-vivo sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said ex-vivo sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, the present invention relates to a method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein for a subject applying to the first gluten-sensitive DQ genotype group (i) the therapeutic regimen comprises one or more of administering the TG2 inhibitor at a higher dose, administering the TG2 inhibitor at higher frequency, longer duration of treatment, administering amore potent TG2 inhibitor than a therapeutic regimen for a subject applying to the second gluten-sensitive DQ genotype group (ii) or third gluten-sensitive DQ genotype group (iii), wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising or consisting of: HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO; wherein step (b) further comprises: identifying said subject as applying to first gluten-sensitive DQ genotype group (i) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.5 I DQ2.5, DQ2.5 I DQ2.3, DQ2.5 / one copy of DQB1*02, or identifying said subject as applying to second gluten-sensitive DQ genotype group (ii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.2 HOMO, DQ8 HOMO, DQ8 / DQ2, DQ2.5 / DQ2.2, or identifying said subject as applying to third gluten-sensitive DQ genotype group (iii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2 half heterodimer, DQ2.2 HETERO, DQ2.5 HETERO, DQ2.5 TrHETERO, DQ8 HETERO, DQ2.5 / one copy of DQA1*05, wherein the TG2 inhibitor is a reversible TG2 inhibitor or an irreversible TG2 inhibitor. In particular preferred embodiments, the transglutaminase 2 inhibitor is (S,E)-methyl-7-(1-(2-(2-ethylbutylamino)-2-oxoethyl)-2-oxo-1,2-dihydro-pyridin-3-ylamino)-6-(1-methyl-1 H-imidazole-5-carboxamido)-7-oxohept-2-enoate (Compound 1). Preferred is a computer-implemented method for selecting a therapy regimen, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining an ex-vivo sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said ex-vivo sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO, wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -0.7 to -3.0 (-0.7 > VH:CrD ratio > -3.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -1.3 (-0.1 > VH:CrD ratio > -1.3) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.05 to -0.7 (-0.05 > VH:CrD ratio > -0.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet; preferably wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.4 to -1.0 (-0.4 > VH:CrD ratio > -1.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -0.4 (-0.1 > VH:CrD ratio > -0.4) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Preferred is a method, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining a sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Thus, in embodiments wherein wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -0.7 to -3.0 (-0.7 > VH:CrD ratio > -3.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -1.3 (-0.1 > VH:CrD ratio > -1.3) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.05 to -0.7 (-0.05 > VH:CrD ratio > -0.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet; preferably wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.4 to -1.0 (-0.4 > VH:CrD ratio > -1.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -0.4 (-0.1 > VH:CrD ratio > -0.4) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, step b) preferably comprises: (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.7 to -3.0, preferably between -1.0 to -2.7 from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet; wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.1 to -1.3, between -0.4 to -1.0 from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet; wherein third gluten-sensitive DQ genotype group has a gluten-specific T cell response characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.05 to -0.7, preferably between -0.1 to -0.4 from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation. Moreover, a subject applying to the first gluten-sensitive DQ genotype group receiving a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of celiac disease is preferably also characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.41 to -0.60 (-0.41 > VH:CrD ratio > -0.60) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Moreover, a subject applying to the second gluten-sensitive DQ genotype group receiving a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of celiac disease is preferably also characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.16 to -0.40 (-0.16 > VH:CrD ratio > -0.40) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Moreover, a subject applying to the third gluten-sensitive DQ genotype group receiving a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of celiac disease is preferably also characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.05 to -0.15 (-0.05 > VH:CrD ratio > -0.15) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein a subject applying to (i) receiving a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of celiac disease is characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.41 to -0.60 (-0.41 > VH:CrD ratio > -0.60) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) receiving a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of celiac disease is characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.16 to -0.40 (-0.16 > VH:CrD ratio > -0.40) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) receiving a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of celiac disease is characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.05 to -0.15 (-0.05 > VH:CrD ratio > -0.15) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO, wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -0.7 to -3.0 (-0.7 > VH:CrD ratio > -3.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -1.3 (-0.1 > VH:CrD ratio > -1.3) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.05 to -0.7 (-0.05 > VH:CrD ratio > -0.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Preferred is a method, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining a sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a’) obtaining an ex-vivo sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said ex-vivo sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject, (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 I HLA-DQ2.2, HLA-DQ2.3 I HLA-DQ2.3, HLA-DQ2.5 I HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO, wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -0.7 to -3.0 (-0.7 > VH:CrD ratio > -3.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -1.3 (-0.1 > VH:CrD ratio > -1.3) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.05 to -0.7 (-0.05 > VH:CrD ratio > -0.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet; preferably wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.4 to -1.0 (-0.4 > VH:CrD ratio > -1.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -0.4 (-0.1 > VH:CrD ratio > -0.4) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, wherein the TG2 inhibitor is a reversible TG2 inhibitor or an irreversible TG2 inhibitor. In particular preferred embodiments, the transglutaminase 2 inhibitor is (S,E)-methyl-7-(1-(2-(2-ethylbutylamino)-2-oxoethyl)-2-oxo-1,2-dihydro-pyridin-3-ylamino)-6-(1-methyl-1 H-imidazole-5-carboxamido)-7-oxohept-2-enoate (Compound 1). Preferred is a method, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining a sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO, wherein step (b) further comprises: identifying said subject as applying to first gluten-sensitive DQ genotype group (i) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.5 I DQ2.5, DQ2.5 I DQ2.3, DQ2.5 / one copy of DQB1*02, or identifying said subject as applying to second gluten-sensitive DQ genotype group (ii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.2 HOMO, DQ8 HOMO, DQ8 / DQ2, DQ2.5 / DQ2.2, or identifying said subject as applying to third gluten-sensitive DQ genotype group (iii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2 half heterodimer, DQ2.2 HETERO, DQ2.5 HETERO, DQ2.5 TrHETERO, DQ8 HETERO, DQ2.5 / one copy of DQA1*05, wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -0.7 to -3.0 (-0.7 > VH:CrD ratio > -3.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -1.3 (-0.1 > VH:CrD ratio > -1.3) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.05 to -0.7 (-0.05 > VH:CrD ratio > -0.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, preferably wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.4 to -1.0 (-0.4 > VH:CrD ratio > -1.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -0.4 (-0.1 > VH:CrD ratio > -0.4) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Preferred is a method, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining a sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen selected from one or more therapeutic measures comprising a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein for a subject applying to the first gluten-sensitive DQ genotype group (i) the therapeutic regimen comprises one or more of administering the TG2 inhibitor at a higher dose, administering the TG2 inhibitor at higher frequency, longer duration of treatment, administering a more potent TG2 inhibitor than a therapeutic regimen for a subject applying to the second gluten-sensitive DQ genotype group (ii) or third gluten-sensitive DQ genotype group (iii), wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO, wherein step (b) further comprises: identifying said subject as applying to first gluten-sensitive DQ genotype group (i) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.5 I DQ2.5, DQ2.5 I DQ2.3, DQ2.5 / one copy of DQB1*02, or identifying said subject as applying to second gluten-sensitive DQ genotype group (ii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.2 HOMO, DQ8 HOMO, DQ8 / DQ2, DQ2.5 / DQ2.2, or identifying said subject as applying to third gluten-sensitive DQ genotype group (iii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2 half heterodimer, DQ2.2 HETERO, DQ2.5 HETERO, DQ2.5 TrHETERO, DQ8 HETERO, DQ2.5 / one copy of DQA1*05, wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -0.7 to -3.0 (-0.7 > VH:CrD ratio > -3.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -1.3 (-0.1 > VH:CrD ratio > -1.3) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.05 to -0.7 (-0.05 > VH:CrD ratio > -0.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet; preferably wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.4 to -1.0 (-0.4 > VH:CrD ratio > -1.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -0.4 (-0.1 > VH:CrD ratio > -0.4) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Preferred is a method, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining a sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a’) obtaining an ex-vivo sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said ex-vivo sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject, (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein for a subject applying to the first gluten-sensitive DQ genotype group (i) the therapeutic regimen comprises one or more of administering the TG2 inhibitor at a higher dose, administering the TG2 inhibitor at higher frequency, longer duration of treatment, administering a more potent TG2 inhibitor than a therapeutic regimen for a subject applying to the second gluten-sensitive DQ genotype group (ii) or third gluten-sensitive DQ genotype group (iii), wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO, wherein step (b) further comprises: identifying said subject as applying to first gluten-sensitive DQ genotype group (i) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.5 I DQ2.5, DQ2.5 I DQ2.3, DQ2.5 / one copy of DQB1*02, or identifying said subject as applying to second gluten-sensitive DQ genotype group (ii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.2 HOMO, DQ8 HOMO, DQ8 / DQ2, DQ2.5 / DQ2.2, or identifying said subject as applying to third gluten-sensitive DQ genotype group (iii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2 half heterodimer, DQ2.2 HETERO, DQ2.5 HETERO, DQ2.5 TrHETERO, DQ8 HETERO, DQ2.5 / one copy of DQA1*05, wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -0.7 to -3.0 (-0.7 > VH:CrD ratio > -3.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -1.3 (-0.1 > VH:CrD ratio > -1.3) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.05 to -0.7 (-0.05 > VH:CrD ratio > -0.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet; preferably wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.4 to -1.0 (-0.4 > VH:CrD ratio > -1.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -0.4 (-0.1 > VH:CrD ratio > -0.4) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, wherein the TG2 inhibitor is a reversible TG2 inhibitor or an irreversible TG2 inhibitor. In particular preferred embodiments, the transglutaminase 2 inhibitor is (S,E)-methyl-7-(1-(2-(2-ethylbutylamino)-2-oxoethyl)-2-oxo-1,2-dihydro-pyridin-3-ylamino)-6-(1-methyl-1 H-imidazole-5-carboxamido)-7-oxohept-2-enoate (Compound 1). Preferred is a method, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining a sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 I HLA-DQ2.2, HLA-DQ2.3 I HLA-DQ2.3, HLA-DQ2.5 I HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO, wherein the first gluten-sensitive DQ genotype group has a more dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein more dysregulated genexpression is characterized by at least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 (mature enterocytes) are at least 50% more downregulated in the first glutensensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% - 90%; and / or at least one, preferably more than one of the genes AGR2, MKI167, and CENPF (cell proliferation) are at least 30% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 33% - 100%; and / or at least one, preferably more than one of the genes STAT1, GBP1 and TGM2 (inflammation) are at least 50% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% - 100%; and wherein the second gluten-sensitive DQ genotype group has a more dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein more dysregulated genexpression is characterized by at least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 (mature enterocytes) are between 10% - 49% more downregulated in the second gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group; and / or at least one, preferably more than one of the genes AGR2, MKI167, and CENPF (cell proliferation) are between 10% - 29% more upregulated in the second gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 12% - 25%; and / or at least one, preferably more than one of the genes STAT1, GBP1 and TGM2 (inflammation) are between 1% - 49% more upregulated in the second glutensensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 5% - 20%. Preferably, the therapy regimen preferably comprises TG2 inhibitor at a daily dose between 0.1 mg - 1000 mg, preferably between 0.5 mg - 500 mg, more preferably between 0.75 mg - 250 mg, most preferably between 1 mg - 100 mg. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose between 150 mg - 250 mg, more preferably between 160 mg - 240 mg, more preferably between 170 mg - 230 mg, more preferably between 180 mg - 220 mg, more preferably between 190 mg - 210 mg. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose of (about) 200 mg. More preferably, the therapy regimen for the first gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 25 mg - 1000 mg, preferably between 25 mg - 500 mg, more preferably between 25 mg - 250 mg, most preferably between 30 mg - 100 mg, and / or wherein the therapy regimen for the second gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 5 mg - 750 mg, more preferably between 5 mg - 250 mg, preferably between 5 mg - 75 mg, most preferably between 10 mg - 30 mg, and / or wherein the therapy regimen for the third gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 0.1 mg - 500 mg, more preferably between 0.1 mg - 250 mg, preferably between 0.1 mg - 50 mg, most preferably between 1 mg - 10 mg. In some preferred embodiments, the therapy regimen regimen for the first glutensensitive DQ genotype group preferably comprises TG2 inhibitor at a daily dose between 150 mg - 250 mg, more preferably between 160 mg - 240 mg, more preferably between 170 mg - 230 mg, more preferably between 180 mg - 220 mg, more preferably between 190 mg - 210 mg. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose of (about) 200 mg. Preferred is a method, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining a sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -0.7 to -3.0 (-0.7 > VH:CrD ratio > -3.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -1.3 (-0.1 > VH:CrD ratio > -1.3) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.05 to -0.7 (-0.05 > VH:CrD ratio > -0.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet; preferably wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.4 to -1.0 (-0.4 > VH:CrD ratio > -1.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -0.4 (-0.1 > VH:CrD ratio > -0.4) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Preferred is a method, wherein the first gluten-sensitive DQ genotype group has a more dysregulated group of (at least two) genes of a biological pathway than the third gluten-sensitive DQ genotype group, wherein a more dysregulated group of (at least two) genes of a biological pathway is characterized by for transit amplifying cells, genes from the first gluten-sensitive DQ genotype group are on average at least 50% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for mature enterocytes genes from the first gluten-sensitive DQ genotype group are on average at least 200% more downregulated than genes from the third gluten-sensitive DQ genotype group; and / or for immune cells, genes from the first gluten-sensitive DQ genotype group are on average at least 100% more upregulated than genes from the third glutensensitive DQ genotype group, and / or for duodenal transporter cells, genes from the first gluten-sensitive DQ genotype group are on average at least 200% more upregulated than genes from the third gluten-sensitive DQ genotype group; wherein the second gluten-sensitive DQ genotype group has a more dysregulated group of (at least two) genes of a biological pathway than the third gluten-sensitive DQ genotype group, wherein a more dysregulated group of (at least two) genes of a biological pathway is characterized by for transit amplifying cells, genes from the second gluten-sensitive DQ genotype group are on average at least 20% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for mature enterocytes, genes from the second gluten-sensitive DQ genotype group are on average at least 50% more downregulated than genes from the third gluten-sensitive DQ genotype group; and / or for immune cells, genes from the second gluten-sensitive DQ genotype group are on average at least 5% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for duodenal transporter cells, genes from the second gluten-sensitive DQ genotype group are on average at least 50% more upregulated than genes from the third gluten-sensitive DQ genotype group. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO, wherein the first gluten-sensitive DQ genotype group has a more dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein more dysregulated genexpression is characterized by at least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 (mature enterocytes) are at least 50% more downregulated in the first gluten sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% - 90%; and / or at least one, preferably more than one of the genes AGR2, MKI167, and CENPF (cell proliferation) are at least 30% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 33% - 100%; and / or at least one, preferably more than one of the genes STAT1, GBP1 and TGM2 (inflammation) are at least 50% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% - 100%; and wherein the second gluten-sensitive DQ genotype group has a more dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein stronger dysregulated genexpression is characterized by at least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 (mature enterocytes) are are between 10% - 49% more downregulated in the second gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group; and / or at least one, preferably more than one of the genes AGR2, MKI167, and CENPF (cell proliferation) are between 10% - 29% more upregulated in the second gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 12% - 25%; and / or at least one, preferably more than one of the genes STAT1, GBP1 and TGM2 (inflammation) are between 1% - 49% more upregulated in the second glutensensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 5% - 20%.wherein the TG2 inhibitor is a reversible TG2 inhibitor or an irreversible TG2 inhibitor. Preferred is a method, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining a sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.4 to -1.0 (-0.4 > VH:CrD ratio > -1.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -0.4 (-0.1 > VH:CrD ratio > -0.4) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Preferred is a method, wherein the first gluten-sensitive DQ genotype group has a more dysregulated group of (at least two) genes of a biological pathway than the third gluten-sensitive DQ genotype group, wherein a more dysregulated group of (at least two) genes of a biological pathway is characterized by for transit amplifying cells, genes from the first gluten-sensitive DQ genotype group are on average at least 50% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for mature enterocytes genes from the first gluten-sensitive DQ genotype group are on average at least 200% more downregulated than genes from the third gluten-sensitive DQ genotype group; and / or for immune cells, genes from the first gluten-sensitive DQ genotype group are on average at least 100% more upregulated than genes from the third glutensensitive DQ genotype group, and / or for duodenal transporter cells, genes from the first gluten-sensitive DQ genotype group are on average at least 200% more upregulated than genes from the third gluten-sensitive DQ genotype group; wherein the second gluten-sensitive DQ genotype group has a more dysregulated group of (at least two) genes of a biological pathway than the third gluten-sensitive DQ genotype group, wherein a more dysregulated group of (at least two) genes of a biological pathway is characterized by for transit amplifying cells, genes from the second gluten-sensitive DQ genotype group are on average at least 20% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for mature enterocytes, genes from the second gluten-sensitive DQ genotype group are on average at least 50% more downregulated than genes from the third gluten-sensitive DQ genotype group; and / or for immune cells, genes from the second gluten-sensitive DQ genotype group are on average at least 5% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for duodenal transporter cells, genes from the second gluten-sensitive DQ genotype group are on average at least 50% more upregulated than genes from the third gluten-sensitive DQ genotype group. In particular preferred embodiments, the transglutaminase 2 inhibitor is (S,E)-methyl-7-(1-(2-(2-ethylbutylamino)-2-oxoethyl)-2-oxo-1,2-dihydro-pyridin-3-ylamino)-6-(1-methyl-1 H-imidazole-5-carboxamido)-7-oxohept-2-enoate (Compound 1). Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO, wherein step (b) further comprises: identifying said subject as applying to first gluten-sensitive DQ genotype group (i) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.5 I DQ2.5, DQ2.5 I DQ2.3, DQ2.5 / one copy of DQB1*02, or identifying said subject as applying to second gluten-sensitive DQ genotype group (ii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.2 HOMO, DQ8 HOMO, DQ8 / DQ2, DQ2.5 / DQ2.2, or identifying said subject as applying to third gluten-sensitive DQ genotype group (iii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2 half heterodimer, DQ2.2 HETERO, DQ2.5 HETERO, DQ2.5 TrHETERO, DQ8 HETERO, DQ2.5 / one copy of DQA1*05, wherein the first gluten-sensitive DQ genotype group has a stronger dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein stronger dysregulated genexpression is characterized by at least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 (mature enterocytes) are at least 50% more downregulated in the first gluten sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% - 90%; and / or at least one, preferably more than one of the genes AGR2, MKI167, and CENPF (cell proliferation) are at least 30% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 33% - 100%; and / or at least one, preferably more than one of the genes STAT1, GBP1 and TGM2 (inflammation) are at least 50% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% - 100%; and wherein the second gluten-sensitive DQ genotype group has a stronger dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein stronger dysregulated genexpression is characterized by at least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 (mature enterocytes) are are between 10% - 49% more downregulated in the second gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group; and / or at least one, preferably more than one of the genes AGR2, MKI167, and CENPF (cell proliferation) are between 10% - 29% more upregulated in the second gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 12% -25%; and / or at least one, preferably more than one of the genes STAT1, GBP1 and TGM2 (inflammation) are between 1% - 49% more upregulated in the second glutensensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 5% - 20%. Preferred is a method, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining a sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.4 to -1.0 (-0.4 > VH:CrD ratio > -1.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -0.4 (-0.1 > VH:CrD ratio > -0.4) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Preferred is a method, wherein the first gluten-sensitive DQ genotype group has a more dysregulated group of (at least two) genes of a biological pathway than the third gluten-sensitive DQ genotype group, wherein a more dysregulated group of (at least two) genes of a biological pathway is characterized by for transit amplifying cells, genes from the first gluten-sensitive DQ genotype group are on average at least 50% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for mature enterocytes genes from the first gluten-sensitive DQ genotype group are on average at least 200% more downregulated than genes from the third gluten-sensitive DQ genotype group; and / or for immune cells, genes from the first gluten-sensitive DQ genotype group are on average at least 100% more upregulated than genes from the third glutensensitive DQ genotype group, and / or for duodenal transporter cells, genes from the first gluten-sensitive DQ genotype group are on average at least 200% more upregulated than genes from the third gluten-sensitive DQ genotype group; wherein the second gluten-sensitive DQ genotype group has a more dysregulated group of (at least two) genes of a biological pathway than the third gluten-sensitive DQ genotype group, wherein a more dysregulated group of (at least two) genes of a biological pathway is characterized by for transit amplifying cells, genes from the second gluten-sensitive DQ genotype group are on average at least 20% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for mature enterocytes, genes from the second gluten-sensitive DQ genotype group are on average at least 50% more downregulated than genes from the third gluten-sensitive DQ genotype group; and / or for immune cells, genes from the second gluten-sensitive DQ genotype group are on average at least 5% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for duodenal transporter cells, genes from the second gluten-sensitive DQ genotype group are on average at least 50% more upregulated than genes from the third gluten-sensitive DQ genotype group. In particular preferred embodiments, the transglutaminase 2 inhibitor is (S,E)-methyl-7-(1-(2-(2-ethylbutylamino)-2-oxoethyl)-2-oxo-1,2-dihydro-pyridin-3-ylamino)-6-(1-methyl-1 H-imidazole-5-carboxamido)-7-oxohept-2-enoate (Compound 1). Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein for a subject applying to the first gluten-sensitive DQ genotype group (i) the therapeutic regimen comprises one or more of administering the TG2 inhibitor at a higher dose, administering the TG2 inhibitor at higher frequency, longer duration of treatment, administering a more potent TG2 inhibitor than a therapeutic regimen for a subject applying to the second gluten-sensitive DQ genotype group (ii) or third gluten-sensitive DQ genotype group (iii), wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO, wherein step (b) further comprises: identifying said subject as applying to first gluten-sensitive DQ genotype group (i) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.5 I DQ2.5, DQ2.5 I DQ2.3, DQ2.5 / one copy of DQB1*02, or identifying said subject as applying to second gluten-sensitive DQ genotype group (ii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.2 HOMO, DQ8 HOMO, DQ8 / DQ2, DQ2.5 / DQ2.2, or identifying said subject as applying to third gluten-sensitive DQ genotype group (iii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2 half heterodimer, DQ2.2 HETERO, DQ2.5 HETERO, DQ2.5 TrHETERO, DQ8 HETERO, DQ2.5 / one copy of DQA1*05, wherein the first gluten-sensitive DQ genotype group has a stronger dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein stronger dysregulated genexpression is characterized by at least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 (mature enterocytes) are at least 50% more downregulated in the first glutensensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% - 90%; and / or at least one, preferably more than one of the genes AGR2, MKI167, and CENPF (cell proliferation) are at least 30% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 33% - 100%; and / or at least one, preferably more than one of the genes STAT1, GBP1 and TGM2 (inflammation) are at least 50% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% - 100%; and wherein the second gluten-sensitive DQ genotype group has a stronger dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein stronger dysregulated genexpression is characterized by at least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 (mature enterocytes) are are between 10% - 49% more downregulated in the second gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group; and / or at least one, preferably more than one of the genes AGR2, MKI167, and CENPF (cell proliferation) are between 10% - 29% more upregulated in the second gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 12% - 25%; and / or at least one, preferably more than one of the genes STAT1, GBP1 and TGM2 (inflammation) are between 1% - 49% more upregulated in the second glutensensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 5% - 20%. Preferred is a method, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining a sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.4 to -1.0 (-0.4 > VH:CrD ratio > -1.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -0.4 (-0.1 > VH:CrD ratio > -0.4) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Preferred is a method, wherein the first gluten-sensitive DQ genotype group has a more dysregulated group of (at least two) genes of a biological pathway than the third gluten-sensitive DQ genotype group, wherein a more dysregulated group of (at least two) genes of a biological pathway is characterized by for transit amplifying cells, genes from the first gluten-sensitive DQ genotype group are on average at least 50% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for mature enterocytes genes from the first gluten-sensitive DQ genotype group are on average at least 200% more downregulated than genes from the third gluten-sensitive DQ genotype group; and / or for immune cells, genes from the first gluten-sensitive DQ genotype group are on average at least 100% more upregulated than genes from the third glutensensitive DQ genotype group, and / or for duodenal transporter cells, genes from the first gluten-sensitive DQ genotype group are on average at least 200% more upregulated than genes from the third gluten-sensitive DQ genotype group; wherein the second gluten-sensitive DQ genotype group has a more dysregulated group of (at least two) genes of a biological pathway than the third gluten-sensitive DQ genotype group, wherein a more dysregulated group of (at least two) genes of a biological pathway is characterized by for transit amplifying cells, genes from the second gluten-sensitive DQ genotype group are on average at least 20% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for mature enterocytes, genes from the second gluten-sensitive DQ genotype group are on average at least 50% more downregulated than genes from the third gluten-sensitive DQ genotype group; and / or for immune cells, genes from the second gluten-sensitive DQ genotype group are on average at least 5% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for duodenal transporter cells, genes from the second gluten-sensitive DQ genotype group are on average at least 50% more upregulated than genes from the third gluten-sensitive DQ genotype group. Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO, wherein step (b) further comprises: identifying said subject as applying to first gluten-sensitive DQ genotype group (i) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.5 I DQ2.5, DQ2.5 I DQ2.3, DQ2.5 / one copy of DQB1*02, or identifying said subject as applying to second gluten-sensitive DQ genotype group (ii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.2 HOMO, DQ8 HOMO, DQ8 / DQ2, DQ2.5 / DQ2.2, or identifying said subject as applying to third gluten-sensitive DQ genotype group (iii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2 half heterodimer, DQ2.2 HETERO, DQ2.5 HETERO, DQ2.5 TrHETERO, DQ8 HETERO, DQ2.5 / one copy of DQA1*05, wherein the first gluten-sensitive DQ genotype group has a more dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein more dysregulated genexpression is characterized by at least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 (mature enterocytes) are at least 50% more downregulated in the first glutensensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% - 90%; and / or at least one, preferably more than one of the genes AGR2, MKI167, and CENPF (cell proliferation) are at least 30% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 33% - 100%; and / or at least one, preferably more than one of the genes STAT1, GBP1 and TGM2 (inflammation) are at least 50% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% - 100%; and wherein the second gluten-sensitive DQ genotype group has a more dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein more dysregulated genexpression is characterized by at least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 (mature enterocytes) are are between 10% - 49% more downregulated in the second gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group; and / or at least one, preferably more than one of the genes AGR2, MKI167, and CENPF (cell proliferation) are between 10% - 29% more upregulated in the second gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 12% - 25%; and / or at least one, preferably more than one of the genes STAT1, GBP1 and TGM2 (inflammation) are between 1% - 49% more upregulated in the second glutensensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 5% - 20%,wherein the TG2 inhibitor is a reversible TG2 inhibitor or an irreversible TG2 inhibitor. Preferred is a method, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining a sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.4 to -1.0 (-0.4 > VH:CrD ratio > -1.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -0.4 (-0.1 > VH:CrD ratio > -0.4) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Preferred is a method, wherein the first gluten-sensitive DQ genotype group has a more dysregulated group of (at least two) genes of a biological pathway than the third gluten-sensitive DQ genotype group, wherein a more dysregulated group of (at least two) genes of a biological pathway is characterized by for transit amplifying cells, genes from the first gluten-sensitive DQ genotype group are on average at least 50% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for mature enterocytes genes from the first gluten-sensitive DQ genotype group are on average at least 200% more downregulated than genes from the third gluten-sensitive DQ genotype group; and / or for immune cells, genes from the first gluten-sensitive DQ genotype group are on average at least 100% more upregulated than genes from the third glutensensitive DQ genotype group, and / or for duodenal transporter cells, genes from the first gluten-sensitive DQ genotype group are on average at least 200% more upregulated than genes from the third gluten-sensitive DQ genotype group; wherein the second gluten-sensitive DQ genotype group has a more dysregulated group of (at least two) genes of a biological pathway than the third gluten-sensitive DQ genotype group, wherein a more dysregulated group of (at least two) genes of a biological pathway is characterized by for transit amplifying cells, genes from the second gluten-sensitive DQ genotype group are on average at least 20% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for mature enterocytes, genes from the second gluten-sensitive DQ genotype group are on average at least 50% more downregulated than genes from the third gluten-sensitive DQ genotype group; and / or for immune cells, genes from the second gluten-sensitive DQ genotype group are on average at least 5% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for duodenal transporter cells, genes from the second gluten-sensitive DQ genotype group are on average at least 50% more upregulated than genes from the third gluten-sensitive DQ genotype group. In particular preferred embodiments, the transglutaminase 2 inhibitor is (S,E)-methyl-7-(1-(2-(2-ethylbutylamino)-2-oxoethyl)-2-oxo-1,2-dihydro-pyridin-3-ylamino)-6-(1-methyl-1 H-imidazole-5-carboxamido)-7-oxohept-2-enoate (Compound 1). Preferably, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein for a subject applying to the first gluten-sensitive DQ genotype group (i) the therapeutic regimen comprises one or more of administering the TG2 inhibitor at a higher dose, administering the TG2 inhibitor at higher frequency, longer duration of treatment, administering a more potent TG2 inhibitor than a therapeutic regimen for a subject applying to the second gluten-sensitive DQ genotype group (ii) or third gluten-sensitive DQ genotype group (iii), wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO, wherein the first gluten-sensitive DQ genotype group has a more dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein more dysregulated genexpression is characterized by at least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 (mature enterocytes) are at least 50% more downregulated in the first glutensensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% - 90%; and / or at least one, preferably more than one of the genes AGR2, MKI167, and CENPF (cell proliferation) are at least 30% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 33% - 100%; and / or at least one, preferably more than one of the genes STAT1, GBP1 and TGM2 (inflammation) are at least 50% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% - 100%; and wherein the second gluten-sensitive DQ genotype group has a more dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein more dysregulated genexpression is characterized by at least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 (mature enterocytes) are are between 10% - 49% more downregulated in the second gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group; and / or at least one, preferably more than one of the genes AGR2, MKI167, and CENPF (cell proliferation) are between 10% - 29% more upregulated in the second gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 12% - 25%; and / or at least one, preferably more than one of the genes STAT1, GBP1 and TGM2 (inflammation) are between 1% - 49% more upregulated in the second glutensensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 5% - 20%, wherein the TG2 inhibitor is a reversible TG2 inhibitor or an irreversible TG2 inhibitor. Preferred is a method, wherein before step (a) the method further comprises steps (a’) and (a”): (a’) obtaining a sample of genetic material from said subject; (a”) determining the human leukocyte antigen class II genotype of said subject in said sample of genetic material, wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject. Preferably, wherein a subject applying to (i) is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (ii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.4 to -1.0 (-0.4 > VH:CrD ratio > -1.0) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet, and / or wherein a subject applying to (iii) is characterized by a villous height to crypt depth (VH:CrD) ratio between -0.1 to -0.4 (-0.1 > VH:CrD ratio > -0.4) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Preferred is a method, wherein the first gluten-sensitive DQ genotype group has a more dysregulated group of (at least two) genes of a biological pathway than the third gluten-sensitive DQ genotype group, wherein a more dysregulated group of (at least two) genes of a biological pathway is characterized by for transit amplifying cells, genes from the first gluten-sensitive DQ genotype group are on average at least 50% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for mature enterocytes genes from the first gluten-sensitive DQ genotype group are on average at least 200% more downregulated than genes from the third gluten-sensitive DQ genotype group; and / or for immune cells, genes from the first gluten-sensitive DQ genotype group are on average at least 100% more upregulated than genes from the third glutensensitive DQ genotype group, and / or for duodenal transporter cells, genes from the first gluten-sensitive DQ genotype group are on average at least 200% more upregulated than genes from the third gluten-sensitive DQ genotype group; wherein the second gluten-sensitive DQ genotype group has a more dysregulated group of (at least two) genes of a biological pathway than the third gluten-sensitive DQ genotype group, wherein a more dysregulated group of (at least two) genes of a biological pathway is characterized by for transit amplifying cells, genes from the second gluten-sensitive DQ genotype group are on average at least 20% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for mature enterocytes, genes from the second gluten-sensitive DQ genotype group are on average at least 50% more downregulated than genes from the third gluten-sensitive DQ genotype group; and / or for immune cells, genes from the second gluten-sensitive DQ genotype group are on average at least 5% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / or for duodenal transporter cells, genes from the second gluten-sensitive DQ genotype group are on average at least 50% more upregulated than genes from the third gluten-sensitive DQ genotype group. In particular preferred embodiments, the transglutaminase 2 inhibitor is (S,E)-methyl-7-(1-(2-(2-ethylbutylamino)-2-oxoethyl)-2-oxo-1,2-dihydro-pyridin-3-yl-amino)-6-(1-methyl-1 H-imidazole-5-carboxamido)-7-oxohept-2-enoate (Comp. 1). The present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein step b) further comprises identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to the first gluten-sensitive DQ genotype group, if the subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease. Preferably, a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. The present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger glutenspecific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger glutenspecific T cell response than the third gluten-sensitive DQ genotype group, wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to (encoding proteins for) mature enterocytes and / or cell proliferation and / or inflammation; and (c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject, wherein one or more therapeutic measures comprising dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, duration of treatment, of the therapy regimen differ based on the DQ genotype group (i), (ii), or (iii) of said subject, with other words wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subject, wherein a subject applying to the first gluten-sensitive DQ genotype group is a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease. Preferably, a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. Thus, the present invention relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease; (c) selecting or adjusting a therapy regimen for said subject if the subject has been identified having a risk for refractory coeliac diseases or suffering from refractory coeliac diseases , wherein the therapy regimen comprises one or more therapeutic measures selected from dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, and duration of treatment. The present invention further relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease; (c) selecting or adjusting a therapy regimen for said subject if the subject has been identified having a risk for refractory coeliac diseases or suffering from refractory coeliac diseases, wherein the therapy regimen comprises one or more therapeutic measures selected from dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, and duration of treatment, wherein the therapy regimen comprises TG2 inhibitor at a daily dose between 0.1 mg - 1000 mg, preferably between 0.5 mg - 500 mg, more preferably between 0.75 mg - 250 mg, most preferably between 1 mg - 100 mg. Preferably, a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. The present invention further relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease; (c) selecting or adjusting a therapy regimen for said subject if the subject has been identified having a risk for refractory coeliac diseases or suffering from refractory coeliac diseases , wherein the therapy regimen comprises one or more therapeutic measures selected from dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, and duration of treatment, wherein the therapy regimen comprises TG2 inhibitor at a daily dose between 25 mg - 1000 mg, preferably between 25 mg - 500 mg, more preferably between 25 mg - 250 mg, most preferably between 30 mg - 100 mg. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose between 150 mg - 250 mg, more preferably between 160 mg - 240 mg, more preferably between 170 mg - 230 mg, more preferably between 180 mg - 220 mg, more preferably between 190 mg - 210 mg. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose of (about) 200 mg. Preferably, a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. The present invention further relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease; (c) selecting or adjusting a therapy regimen for said subject if the subject has been identified having a risk for refractory coeliac diseases or suffering from refractory coeliac disease, wherein the therapy regimen comprises one or more therapeutic measures selected from dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, and duration of treatment, wherein for a subject having a risk for refractory coeliac disease or suffering from refractory coeliac disease the therapeutic regimen comprises one or more of administering the TG2 inhibitor at a higher dose, administering the TG2 inhibitor at higher frequency, longer duration of treatment, administering a stronger TG2 inhibitor than a therapeutic regimen for a subject not suffering from refractory coeliac disease. Preferably, a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. The present invention further relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease; (c) selecting or adjusting a therapy regimen for said subject if the subject has been identified having a risk for refractory coeliac diseases or suffering from refractory coeliac disease, wherein the therapy regimen comprises one or more therapeutic measures selected from dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, and duration of treatment, wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes. Preferably, a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. The present invention further relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease; (c) selecting or adjusting a therapy regimen for said subject if the subject has been identified having a risk for refractory coeliac diseases or suffering from refractory coeliac disease, wherein the therapy regimen comprises one or more therapeutic measures selected from dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, and duration of treatment, wherein the therapy regimen comprises TG2 inhibitor at a daily dose between 0.1 mg - 1000 mg, preferably between 0.5 mg - 500 mg, most preferably between 1 mg - 100 mg, preferably wherein the therapy regimen comprises TG2 inhibitor at a daily dose between 25 mg - 1000 mg, preferably between 25 mg - 500 mg, more preferably between 25 mg - 250 mg, most preferably between 30 mg - 100 mg; wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose between 150 mg - 250 mg, more preferably between 160 mg - 240 mg, more preferably between 170 mg - 230 mg, more preferably between 180 mg - 220 mg, more preferably between 190 mg - 210 mg. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose of (about) 200 mg. The present invention further relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease; (c) selecting or adjusting a therapy regimen for said subject if the subject has been identified having a risk for refractory coeliac diseases or suffering from refractory coeliac disease, wherein the therapy regimen comprises one or more therapeutic measures selected from dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, and duration of treatment, wherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; and wherein the HLA-DQ8 haplotypes are selected from the group comprising or consisting of: HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 / one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO. Preferably, a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. The present invention further relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease; (c) selecting or adjusting a therapy regimen for said subject if the subject has been identified having a risk for refractory coeliac disease or suffering from refractory coeliac disease, wherein the therapy regimen comprises one or more therapeutic measures selected from dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, and duration of treatment, wherein step b) further comprises identifying said subject as subject having a risk for refractory coeliac disease or suffering from refractory coeliac disease if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.5 / DQ2.5, DQ2.5 / DQ2.3, DQ2.5 / one copy of DQB1 *02. Preferably, a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. The present invention further relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease; (c) selecting or adjusting a therapy regimen for said subject if the subject has been identified having a risk for refractory coeliac disease or suffering from refractory coeliac disease, wherein the therapy regimen comprises one or more therapeutic measures selected from dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, and duration of treatment, wherein the therapy regimen comprises TG2 inhibitor at a daily dose between 0.1 mg - 1000 mg, preferably between 0.5 mg - 500 mg, most preferably between 1 mg - 100 mg, preferably wherein the therapy regimen comprises TG2 inhibitor at a daily dose between 25 mg - 1000 mg, preferably between 25 mg - 500 mg, more preferably between 25 mg - 250 mg, most preferably between 30 mg - 100 mg; wherein step b) further comprises identifying said subject as subject having a risk for refractory coeliac disease or suffering from refractory coeliac disease if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.5 / DQ2.5, DQ2.5 / DQ2.3, DQ2.5 / one copy of DQB1 *02. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose between 150 mg - 250 mg, more preferably between 160 mg - 240 mg, more preferably between 170 mg - 230 mg, more preferably between 180 mg - 220 mg, more preferably between 190 mg - 210 mg. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose of (about) 200 mg. Preferably, a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. The present invention further relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease; (c) selecting or adjusting a therapy regimen for said subject if the subject has been identified having a risk for refractory coeliac disease or suffering from refractory coeliac disease, wherein the therapy regimen comprises one or more therapeutic measures selected from dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, and duration of treatment, wherein the TG2 inhibitor is a reversible TG2 inhibitor or an irreversible TG2 inhibitor. Preferably, a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. In particular preferred embodiments, the transglutaminase 2 inhibitor is (S,E)-methyl-7-(1-(2-(2-ethylbutylamino)-2-oxoethyl)-2-oxo-1,2-dihydro-pyridin-3-yl-amino)-6-(1-methyl-1 H-imidazole-5-carboxamido)-7-oxohept-2-enoate (Comp. 1). The present invention further relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease; (c) selecting or adjusting a therapy regimen for said subject if the subject has been identified having a risk for refractory coeliac disease or suffering from refractory coeliac disease, wherein the therapy regimen comprises one or more therapeutic measures selected from dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, and duration of treatment, wherein the therapy regimen comprises TG2 inhibitor at a daily dose between 0.1 mg - 1000 mg, preferably between 0.5 mg - 500 mg, most preferably between 1 mg - 100 mg, preferably wherein the therapy regimen comprises TG2 inhibitor at a daily dose between 25 mg - 1000 mg, preferably between 25 mg - 500 mg, more preferably between 25 mg - 250 mg, most preferably between 30 mg - 100 mg; wherein the TG2 inhibitor is a reversible TG2 inhibitor or an irreversible TG2 inhibitor. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose between 150 mg - 250 mg, more preferably between 160 mg - 240 mg, more preferably between 170 mg - 230 mg, more preferably between 180 mg - 220 mg, more preferably between 190 mg - 210 mg. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose of (about) 200 mg. Preferably, a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. In particular preferred embodiments, the transglutaminase 2 inhibitor is (S,E)-methyl-7-(1-(2-(2-ethylbutylamino)-2-oxoethyl)-2-oxo-1,2-dihydro-pyridin-3-yl-amino)-6-(1-methyl-1 H-imidazole-5-carboxamido)-7-oxohept-2-enoate (Comp. 1). The present invention further relates to a computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, or formulated differently wherein the therapy regimen comprises at least the treatment of celiac disease by administering a therapeutically effective amount of at least one TG2 inhibitor to said subject, the method comprising: (a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject; (b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease; (c) selecting or adjusting a therapy regimen for said subject if the subject has been identified having a risk for refractory coeliac disease or suffering from refractory coeliac disease, wherein the therapy regimen comprises one or more therapeutic measures selected from dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, and duration of treatment, wherein the therapy regimen comprises TG2 inhibitor at a daily dose between 0.1 mg - 1000 mg, preferably between 0.5 mg - 500 mg, most preferably between 1 mg - 100 mg, preferably wherein the therapy regimen comprises TG2 inhibitor at a daily dose between 25 mg - 1000 mg, preferably between 25 mg - 500 mg, more preferably between 25 mg - 250 mg, most preferably between 30 mg - 100 mg; wherein the TG2 inhibitor is a reversible TG2 inhibitor or an irreversible TG2 inhibitor, wherein step b) further comprises identifying said subject as subject having a risk for refractory coeliac disease or suffering from refractory coeliac disease if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.5 / DQ2.5, DQ2.5 / DQ2.3, DQ2.5 / one copy of DQB1 *02. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose between 150 mg - 250 mg, more preferably between 160 mg - 240 mg, more preferably between 170 mg - 230 mg, more preferably between 180 mg - 220 mg, more preferably between 190 mg - 210 mg. In some preferred embodiments, the therapy regimen preferably comprises TG2 inhibitor at a daily dose of (about) 200 mg. Preferably, a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet. In particular preferred embodiments, the transglutaminase 2 inhibitor is (S,E)-methyl-7-(1-(2-(2-ethylbutylamino)-2-oxoethyl)-2-oxo-1,2-dihydro-pyridin-3-ylamino)-6-(1-methyl-1 H-imidazole-5-carboxamido)-7-oxohept-2-enoate (Compound 1). TG2 Inhibitor The TG2 inhibitor may be a reversible TG2 inhibitor or an irreversible TG2 inhibitor. In some preferred embodiments, the TG2 inhibitor is a reversible TG2 inhibitor. In some preferred embodiments, the TG2 inhibitor is an irreversible TG2 inhibitor. Reversible TG2 Inhibitors 1) Reversible Inhibitors In some preferred embodiments the TG2 inhibitor is a reversible TG2 inhibitor. In some further preferred embodiments, the reversible TG2 inhibitor is a compound of the general formula (lrev): R1 wherein L represents -L1- or -L1-L2-; preferably -L1-L2-; L1 represents -CH^, -CH2CH2-, -CH2CH2CH2-, -CH2CO-, or -CH2CH2CO-; L2 represents a bond, -NRN1-, -NRn1CH2-, -NRn1CH2CH2-, or -NRn1CH(CH3)-; wherein the unsubstituted bicyclic residues can be substituted with 1 to 5 of the substituents R9 - R14 and RN ; and preferably with 1 to 3 of the substituents R11 -R13; R3 represents bicyclo[1.1.1 ]pentyl, bicyclo[2.1,1]hexyl, bicyclo[2.2.1]heptyl, bicyclo[3.1,1]heptyl, bicyclo[2.2.2]octyl, bicyclo[3.2.1]octyl, bicyclo[3.2.2]nonyl, bicyclo[3.3.2]decyl, bicyclo[3.3.3]undecyl, 4-homoisotwistyl, adamantyl, diamantyl, hexamethylenetetraminyl and the afore-mentioned residues optionally contain one or more C=C double bond(s) and / or are optionally substituted by one or more of Ra, Rb, Rc, Rd, and Re; Ra, Rb, Rc, Rd, and Re represent independently of each other -H, -F, -Cl, -Br, -CN, -OH, -CH3, -CH2CH3, -CH2CH2CH3, -CH(CH3)2, -CHF2i -CF3, -CH2CF3, -COCH3, -COCH2CH3, -CO2H, -CO2CH3, -CO2C2H5, -CONH2, -CONHCH3, -CON(CH3)2, -CONHC2H5, -CH2CO2H, -CH2CO2CH3, -CH2CO2C2H5, -CH2CONH2, -CH2CONHCH3, -CH2CON(CH3)2, -CH2CONHC2H5, -NHCOCH3, -NHCOC2H5, -NHCOCF3, -NHCOCH2CF3, -NHSO2CH3, -NHSO2C2H5, -NHSO2CHF2, -NHSO2CF3, or -NHSO2CH2CF3; R4 represents -NR6R7; R6 and R7 represent independently of each other -H,   -CH3, -CH2CH3, -CH2CH2CH3, -CH(CH3)2, -CH2CH2CH2CH3, -CH2CH2CH2CH2CH3, -CH2CH(CH3)2,      -C(CH3)3, -CH2CH=CH2, -CH2CH=CH(CH3), -CH2CH=C(CH3)2, -CH2CH=CHCH2CH3, -cyclo-C3H5, -cyclo-C4H7, -cyclo-CsHg, -cyclo-CeHn, -CH2-cyclo-C3H5, -CH2-cyclo-C4H7, -CH2-cyclo-C5H9, -CH2-cyclo-C6Hn, -Ph, -CH2-Ph, -CH2OCH3, -CH2OCH2CH3, -CH2CH2OCH3, -CH2CH2OCH2CH3, -CH2CH2NHCH3, or -CH2CH2N(CH3)2, or-NR6R7 is -N(C2H5)2, R8, R9, R10, R11, R12, R13, and R14 represent independently of each other -H, -F, -Cl, -Br, -I, -OH, -CN, -NO2, -CH3, -C2H5, -C3H7, -CH(CH3)2,     -C4H9,     -CH2-CH(CH3)2, -CH(CH3)-C2H5,     -C(CH3)3, -cyclo-C3H5, -CH2-cyclo-C3H5, -CH2OH, -CH2F, -CHF2, -CF3, -CH2CI, -CH2Br, -CH2I, -CH2-CH2F, -CH2-CHF2, -CH2-CF3, -CH2-CH2CI, -CH2-CH2Br, -CH2-CH2I, -OCH3, -OC2H5,   -OC3H7,   -OCH(CH3)2, -OC(CH3)3, -OC4H9, -OCHF2, -OCF3, -OCH2CF3, -OC2F5, -OCH2OCH3, —O-cyclo-CsHs,      — OCH2-cyclo-C3H5,      —O—C2H4-cyclo-C3H5,      —CHO, -COCH3, -COCF3, -COC2H5, -COC3H7, -COCH(CH3)2, -COC(CH3)3, -COOH, -COOCH3, -COOC2H5, -COOC3H7, -COOCH(CH3)2, -COOC(CH3)3, -OOC-CH3, -OOC-CF3, -OOC-C2H5, -OOC-C3H7, -OOC-CH(CH3)2, -OOC-C(CH3)3, -NH2, -NHCH3, -NHC2H5, -NHC3H7, -NHCH(CH3)2, -NHC(CH3)3, -N(CH3)2, -N(C2H5)2, -N(C3H7)2, -N[CH(CH3)2]2, -N[C(CH3)3]2, -NHCOCH3, -NHCOCF3, -NHCOC2H5, -NHCOC3H7, -NHCOCH(CH3)2, -NHCOC(CH3)3, -CONH2, -CONHCH3, -CONHC2H5, -CONHC3H7, -CONHCH(CH3)2, -CONH-cyclo-C3H5, -CONHC(CH3)3, -CON(CH3)2, -CON(C2H5)2, -CON(C3H7)2, -CON[CH(CH3)2]2, -CON[C(CH3)3]2, -SO2NH2, -SO2NHCH3, -SO2NHC2H5, -SO2NHC3H7, -SO2NHCH(CH3)2, -SO2NH-cyclo-C3H5, -SO2NHC(CH3)3, -SO2N(CH3)2,    -SO2N(C2H5)2, -SO2N(C3H7)2,     -SO2N[CH(CH3)2]2,     -SO2N[C(CH3)3]2, -NHSO2CH3, -NHSO2CF3, -NHSO2C2H5, -NHSO2C3H7, -NHSO2CH(CH3)2, -NHSO2C(CH3)3, -CH=CH2i -CH2-CH=CH2, -C(CH3)=CH2, -ch=ch-ch3, -C=CH, -C=C-CH3, -CH2-C=CH, -Ph, -O-Ph, -O-CH2-Ph, or R8 and R9 or R9 and R10 can form together one of the following fivemembered or six-membered rings: or R12 and R13 or R13 and R14 can form together one of the following five- membered or six-membered rings: RN represents -H,    -CH3,    -C2H5,    -C3H7,    -CH(CH3)2,    -C4H9, -CH2-CH(CH3)2,   -CH(CH3)-C2H5,   -C(CH3)3,   -cyclo-C3H5,   -cyclo-C4H7, —cyclo-CsHg, —CH2—cyclo—C3H5, — CH2—cyclo-C4H7, —CH2—cyclo-CsHg, — CH2F, -CHF2, -CF3, -CH2CI, -CH2Br, -CH2I,   -CH2-CH2F,   -CH2-CHF2, -CH2-CF3, -CH2-CH2CI, -CH2-CH2Br, -CH2-CH2I, -CH2-CH=CH2, -CH2-CeCH, -CHO, -COCH3, -COC2H5,   -COC3H7,   -COCH(CH3)2, —COC(CH3)3, -CO-cyclo-CsHs, -CO-cyclo-C4H7, -CO-cyclo-CsHg, — COOCH3, -COOC2H5, -COOC3H7, -COOCH(CH3)2, -COOC(CH3)3, -COOCH2Ph, -SO2CH3, -SO2CF3i -SO2C2H5i     -SO2C3H7,     -SO2CH(CH3)2i —SO2-cyclo—C3H5, or —SO2C(CH3)3; RN1 represents -H, -CH3, or -CH2CH3; or a diastereomer, an enantiomer, a mixture of diastereomers, a mixture of enantiomers, a racemate, a solvate, a hydrate, or a pharmaceutically acceptable salt thereof. More preferably, the reversible TG2 inhibitor is a compound of the general formula (lrev), wherein R2 represents wherein the unsubstituted bicyclic residues can be substituted with 1 to 5 of the substituents R9 - R14 and RN ; and preferably with 1 to 3 of the substituents R11 -R13 and the substituents R9 - R14 and RN have the meanings as defined herein for 5 compound of general formula (lrev)- More preferably, the reversible TG2 inhibitor is a compound of the general formula (lrev), wherein R2 represents wherein the unsubstituted bicyclic residues can be substituted with 1 to 5 of the substituents R9 - R14 and RN ; and preferably with 1 to 3 of the substituents R11 -R13 and the substituents R9 - R14 and RN have the meanings as defined herein for a compound of the general formula (lrev)- More preferably, the reversible TG2 inhibitor is a compound of the general formula (lrev), wherein the compound has the formula (lbrev) 0 (lbrev) 10 wherein L represents -L1- or -L1-L2-; preferably -L1-L2-; L1 represents -CH^, -CH2CH2-, -CH2CH2CH2-, -CH2CO-, or -CH2CH2CO-; L2 represents a bond, -NRN1-, -NRn1CH2-, -NRn1CH2CH2-, or -NRn1CH(CH3)-; R3 represents bicyclo[1.1.1 ]pentyl, bicyclo[2.1,1]hexyl, bicyclo[2.2.1]heptyl, bicyclo[3.1,1]heptyl, bicyclo[2.2.2]octyl, bicyclo[3.2.1]octyl, bicyclo[3.2.2]nonyl, bicyclo[3.3.2]decyl, bicyclo[3.3.3]undecyl, 4-homoisotwistyl, adamantyl, diamantyl, hexamethylenetetraminyl, and the afore-mentioned residues optionally contain one or more C=C double bond(s) and / or are substituted by one or more of Ra, Rb, Rc, Rd, and Re; Ra, Rb, Rc, Rd, and Re represent independently of each other -H, -F, -Cl, -Br, -CN, -OH, -CH3, -CH2CH3, -CH2CH2CH3, -CH(CH3)2, -CHF2i -CF3, -CH2CF3, -COCH3, -COCH2CH3, -CO2H, -CO2CH3, -CO2C2H5, -CONH2, -CONHCH3, -CON(CH3)2, -CONHC2H5, -CH2CO2H, -CH2CO2CH3, -CH2CO2C2H5, -CH2CONH2, -CH2CONHCH3, -CH2CON(CH3)2, -CH2CONHC2H5, -NHCOCH3, -NHCOC2H5, -NHCOCF3, -NHCOCH2CF3, -NHSO2CH3, -NHSO2C2H5, -NHSO2CHF2, -NHSO2CF3, or -NHSO2CH2CF3; R4 represents -NR6R7; R6 and R7 represent independently of each other -H,   -CH3, -CH2CH3, -CH2CH2CH3, -CH(CH3)2, -CH2CH2CH2CH3, -CH2CH2CH2CH2CH3, -CH2CH(CH3)2,      -C(CH3)3, -CH2CH=CH2, -CH2CH=CH(CH3), -CH2CH=C(CH3)2, -CH2CH=CHCH2CH3, -cyclo-C3H5, -cyclo-C4H7, -cyclo-CsHg, -cyclo-CeHn, -CH2-cyclo-C3H5, -CH2-cyclo-C4H7, -CH2-cyclo-C5H9, -CH2-cyclo-C6Hn, -Ph, -CH2-Ph, -CH2OCH3, -CH2OCH2CH3, -CH2CH2OCH3, -CH2CH2OCH2CH3, -CH2CH2NHCH3, -CH2CH2N(CH3)2, or -NR6R7 is -N(C2H5)2, RN represents -H,    -CH3,    -C2H5,    -C3H7,    -CH(CH3)2,    -C4H9, -CH2-CH(CH3)2,   -CH(CH3)-C2H5,   -C(CH3)3, -cyclo-C3H5, -cyclo-C4H7, -cyclo-C5H9, -CH2-cyclo-C3H5, -CH2F, -CHF2, -CF3, -CH2CI, -CH2Br, -CH2I, -CH2-CH2F, -CH2-CHF2, -CH2-CF3, -CH2-CH2CI, -CH2-CH2Br, -CH2-CH2I, -CH2-CH=CH2, -CH2-C=CH, -CHO, -COCH3, -COC2H5, -COC3H7, -COCH(CH3)2, -COC(CH3)3, -COOCH3, -COOC2H5, -COOC3H7, -COOCH(CH3)2, -COOC(CH3)3, -COOCH2Ph, -SO2CH3, -SO2CF3, -SO2C2H5, -SO2C3H7, -SO2CH(CH3)2, or -SO2C(CH3)3; RN1 represent -H, -CH3, or -CH2CH3; and R8 - R14 have the meanings as defined in formula (lrev); or a diastereomer, an enantiomer, a mixture of diastereomers, a mixture of enantiomers, a racemate, a solvate, a hydrate, or a pharmaceutically acceptable salt thereof. More preferably, the reversible TG2 inhibitor is a compound of the general formula (lrev), wherein L1 represents -CH2-, or -CH2CO-; L2 represents a bond, -NRN1-, -NRn1CH2-, or -NRn1CH(CH3)-; R3 represents bicyclo[1.1.1 ]pentyl, bicyclo[2.1,1]hexyl, bicyclo[2.2.1]heptyl, bicyclo[3.1.1 ]heptyl, bicyclo[2.2.2]octyl, 4-homoisotwistyl, adamantyl, or diamantyl, and the afore-mentioned residues optionally contain one or more C=C double bond(s) and / or are substituted by one or more of Ra, Rb, Rc, Rd, and Re; and Ra, Rb, Rc, Rd, Re and RN1 have the same meanings as defined herein for compound of the general formula (lrev)- More preferably, the reversible TG2 inhibitor is a compound of the general formula (Lev), wherein R2 represents and R8 - R14 and RN have the meanings as defined herein for a compound of the 5 general formula (lrev)- More preferably, the reversible TG2 inhibitor is a compound of the general formula (lrev), wherein the compound has any one of the formulae (IV-arev) - (IV-orev) and (V-arev) — (V-drev): (IV-erev) (IV-drev) (IV-frev) (IV-hrev) (IV-jrev) (IV-krev) (IV-mrev) (IV-nrev) (IV-Orev) (V-Crev) (V-brev) O (V-drev) and R2, R3, R6, R8, R9, R10, R11, R12, R13, Ra, Rb, Rc, Rd and L2 have the same meanings as defined herein for a reversible TG2 inhibitor is a compound of the general formula (lrev). More preferably, the reversible TG2 inhibitor is a compound of the general formula (lrev), wherein R2 represents 10 R6 represents -H, -CH3, -CH2CH3, -CH(CH3)2, -CH2CH2CH3, -CH2CH=CH2, -CH2CH2CH2CH3, -CH2CH(CH3)2,     -C(CH3)3, -CH2CH2CH2CH2CH3, -cyclo-CsHs, -cyclo-CsHg, -cyclo-CeHn or -CH2-cyclo-C3H5. In some preferred embodiments, the reversible TG2 inhibitor is a compound of the general formula (lrev) selected from the group consisting of: Compound Name II-2: (S)-2-(benzofuran-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2- oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-3: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)- N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide II-4: (S)-2-(3-chlorobenzofuran-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-5: (S)-2-(4-bromobenzofuran-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-6: (S)-2-(4-bromobenzofuran-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-7: (S)-2-(benzo[b]thiophene-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-8: (S)-2-(5-bromobenzo[b]thiophene-2-carboxamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-9: (8)-2-(1 H-indole-2-carboxamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-10: (S)-2-(4,5-difluoro-1 H-indole-2-carboxamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-11: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)- N6-methyl-2-(3-methyl-1 H-indole-2-carboxamido)-5-oxohexanediamide 11-12: (S)-2-(1 H-benzo[d]imidazole-2-carboxamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-13: (S)-2-(2,3-dihydro-1 H-indene-2-carboxamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-14: (S)--(2-bromo-4-methylthiazole-5-carboxamido)-N1 -(1 -(2-(2- adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-15: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)- N6-methyl-2-(4-methyl-2-(trifluoromethyl)thiazole-5-carboxamido)-5- oxohexanediamide 11-16: (S)-2-(4-bromo-2-(trifluoromethyl)thiazole-5-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-17: (S)-2-(2,4-dichlorothiazole-5-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-18: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(2-methoxy-4-methylthiazole-5-carboxamido)-N6-methyl-5-oxohexanediamide 11-19: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(4-methyl-2-phenylthiazole-5-carboxamido)-5-oxohexanediamide II-20: (S)-2-(2,4-dimethylthiazole-5-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-21: (S)-2-(5-bromo-3-methylthiophene-2-carboxamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-22: (S)-2-(3,5-dibromothiophene-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-23: (S)-2-(5-bromothiophene-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-24 (S)-2-(5-chlorothiophene-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-25: (S)-2-(5-bromo-3-methylfuran-2-carboxamido)-N1 -(1 -(2-(2- adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-26 (S)-2-(5-chlorofuran-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-27: (S)-2-(5-chlorothiophene-3-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-28 (S)-2-(2,5-dichlorothiophene-3-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-29 (S)-2-(2,5-dibromothiophene-3-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-30 (S)-2-(5-bromothiophene-3-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-31: (S)-2-(2-chloro-5-methylthiazole-4-carboxamido)-N1 -(1 -(2-(2- adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5- oxohexanediamide II-32: (8)-2-(2,5-dichlorothiazole-4-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-33: (S)-2-(2,5-dibromothiazole-4-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-34 (S)-2-(2-bromo-5-methylthiazole-4-carboxamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-35 (S)-2-(2-bromothiazole-4-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-36 (S)-2-(2-chlorothiazole-4-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-37: (S)-2-(2,5-dimethylfuran-3-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-38: (S)-2-(4,5-dimethylthiazole-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-39 (S)-2-(4-bromothiazole-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-40: (S)-2-(4-bromothiophene-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-41: (S)-2-(4-bromo-3-methylthiophene-2-carboxamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-42: (S)-2-(3-bromothiophene-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-43 (S)-2-(3-chloro-4-methylthiophene-2-carboxamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-44: (S)-2-(4-bromo-5-chlorothiophene-2-carboxamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-45: (S)-2-(4,5-dibromothiophene-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-46 (S)-2-(4,5-dibromo-3-methoxythiophene-2-carboxamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-47: (S)-2-(4-bromofuran-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-48 (8)-2-(4,5-dibromofuran-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-49 (S)-2-(4,5-dichlorothiophene-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-50: (S)-2-((S)-1 -acetylpyrrolidine-2-carboxamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-51: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-d ihydropyridin-3-y I)-N6-methyl-2-(1 -methyl-1 H-1,2,3-triazole-5-carboxamido)-5-oxohexanediamide II-52: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-d ihydropyridin-3-y I)- N6-methyl-5-oxo-2-(2H-tetrazole-5-carboxamido)hexanediamide 11-53 (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-d ihydropyridin-3-y I)-N6-methyl-5-oxo-2-(pyrazine-2-carboxamido)hexanediamide II-54: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-d ihydropyridin-3-y I)-N6-methyl-2-((S)-1-methylpyrrolidine-2-carboxamido)-5-oxohexanediamide II-55: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-d ihydropyridin-3-y I)-N6-methyl-5-oxo-2-((S)-pyrrolidine-3-carboxamido)hexanediamide 11-56 (S)-2-((2S,4S)-4-bromopyrrolidine-2-carboxamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-58 (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-d ihydropyridin-3-y I)-N6-methyl-5-oxo-2-((S)-piperidine-2-carboxamido)hexanediamide 11-59 (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-d ihydropyridin-3-y I)-N6-methyl-5-oxo-2-((R)-piperidine-3-carboxamido)hexanediamide II-60: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-d ihydropyridin-3-y I)-N6-methyl-2-((R)-morpholine-3-carboxamido)-5-oxohexanediamide 11-61: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-d ihydropyridin-3-y I)- N6-methyl-5-oxo-2-(quinuclidine-3-carboxamido)hexanediamide II-62: (S)-methyl             3-(1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2- dihydropyridin-3-ylamino)-6-(methylamino)-1,5,6-trioxohexan-2-ylcarbamoyl)-5-nitrobenzoate 11-63 (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-d ihydropyridin-3-y I)-N6-methyl-2-(5-nitronicotinamido)-5-oxohexanediamide II-64 (8)-5-(1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-ylamino)-6-(methylamino)-1,5,6-trioxohexan-2-ylcarbamoyl)nicotinic acid 11-65 (S)-methyl             5-(1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2- dihydropyridin-3-ylamino)-6-(methylamino)-1,5,6-trioxohexan-2-ylcarbamoyl)nicotinate 11-66 (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-d ihydropyridin-3-y I)- N6-methyl-2-(6-methylimidazo[2,1-b]thiazole-5-carboxamido)-5-oxohexanediamide II-67: (S)-N1 -(1 -(2-(2-adamantyl(methyl)amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-68 (S)-N1 -(1 -(2-(5-hydroxyadamantane-2-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-69 (S)-N1 -(1 -(2-(5-fluoroadamantane-2-amino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide II-70: (S)-N1 -(1 -(2-(5-chloroadamantane-2-amino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-71: (S)-N1 -(1 -(2-(5-bromoadamantane-2-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide II-72: (S)-N1 -(1 -(2-(5-methyladamantane-2-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide II-73: (S)-N1 -(1 -(2-(2-carbonitrileadamantane-2-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide II-74: (S)-N1 -(1 -(2-(2-methyl adamantane-2-carboxylate-2-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2- carboxam ido)-5-oxohexanediam ide II-87: (S)-N1 -(1 -(2-(1 -adamantylmethylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-88 (S)-N1 -(1 -(2-(1 -(1 -adamantyl)ethanamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide II-90: (S)-N1-(1-(2-((1 R,2S,4S)-bicyclo[2.2.1]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediam ide II-92: (S)-N1-methyl-5-(3-methylbenzofuran-2-carboxamido)-2-oxo-N6-(2-oxo-1-(2-oxo-2-((1S,2S,4R)-1,7,7-trimethylbicyclo[2.2.1]heptan-2-ylamino)ethyl)-1,2-dihydropyridin-3-yl)hexanediamide II-94 (S)-N1-(1-(2-((1 R,2R,4S)-bicyclo[2.2.1]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)- 5-oxohexanediam ide 11-95 (S)-N1-(1-(2-(bicyclo[2.2.1]heptan-1-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-96 (S)-N1 -(1 -(2-(bicyclo[2.2.1 ]heptan-7-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide II-97: (S)-N1 -(1 -(2-(bicyclo[2.2.1 ]hept-5-en-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-98 (2S)-N1 -(1 -(2-(bicyclo[2.2.2]octan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-99 (S)-N1-methyl-5-(3-methylbenzofuran-2-carboxamido)-2-oxo-N6-(2-oxo-1-(2-oxo-2-((1 R,2R,4R)-1,7,7-trimethylbicyclo[2.2.1]heptan-2-ylamino)ethyl)-1,2-dihydropyridin-3-yl)hexanediamide 11-100: (S)-N1-methyl-5-(3-methylbenzofuran-2-carboxamido)-2-oxo-N6-(2-oxo-1-(2-oxo-2-((1 R,2R,3R,5S)-2,6,6-trimethylbicyclo[3.1.1 ]heptan-3-ylamino)ethyl)-1,2-dihydropyridin-3-yl)hexanediamide 11-101: (S)-N1-methyl-5-(3-methylbenzofuran-2-carboxamido)-2-oxo-N6-(2-oxo-1-(2-oxo-2-((1 S,2S,3S,5R)-2,6,6-trimethylbicyclo[3.1.1 ]heptan-3-ylamino)ethyl)-1,2-dihydropyridin-3-yl)hexanediamide 11-103: (S)-N1 -(1 -(2-(4-homoisotwistane-3-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-104: (S)-N1 -(1 -(2-(diamantane-1 -amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-105: (S)-N1 -(1 -(2-(diamantane-4-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-107: (S)-N1 -(1 -(1 -adamantylmethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-108: (2S)-N1 -(1 -((3-hydroxy-1 -adamantyl)methyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-109: (2S)-N1-(1-((3-bromo-1-adamantyl)methyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-110: (S)-N1 -(1 -(2-adamantylmethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-111: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)- N6-methyl-2-(nicotinamido)-5-oxohexanediamide 11-112: (S)-2-(isonicotinamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2- dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-113: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)- N6-methyl-5-oxo-2-(pyridazine-4-carboxamido)hexanediamide 11-114: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-d ihydropyridin-3-y I)- N6-methyl-5-oxo-2-(pyridazine-3-carboxamido)hexanediamide 11-115: (S)-N1-cyclopropyl-N6-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(3-methylbenzofuran-2-carboxamido)-2-oxohexanediamide 11-116: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-d ihydropyridin-3-y I)-2-(3-methylbenzofuran-2-carboxamido)-5-oxo-N6-pentylhexanediamide 11-117: (S)-N1-allyl-N6-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(3-methylbenzofuran-2-carboxamido)-2-oxohexanediamide 11-118: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-d ihydropyridin-3-y I)-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-119: (S)-N1-allyl-5-(benzofuran-2-carboxamido)-N6-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2 -oxohexanediamide 11-120: (S)-2-(benzofuran-2-carboxamido)-N6-isopropyl-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide 11-121: (S)-2-(benzofuran-2-carboxamido)-N6-cyclopropyl-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide 11-122: (S)-2-(benzofuran-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxo-N6-phenylhexanediamide 11-123: (S)-2-(benzofuran-2-carboxamido)-N6-benzyl-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide 11-124: (S)-2-(benzofuran-2-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide 11-125: (8)-2-(2,5-dichlorothiophene-3-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide 11-126: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(4-methyl-2-(trifluoromethyl)thiazole-5-carboxamido)-5-oxohexanediamide 11-127: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(1 -methyl-1 H-1,2,3-triazole-5-carboxamido)-5-oxohexanediamide 11-128: (2S)-N1 -(1 -(2-((1 R,2R,4S)-bicyclo[2.2.1 ]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(2,5-dichlorothiophene-3-carboxamido)-N6- methyl-5-oxohexanediamide 11-129: (2S)-N1 -(1 -(2-((1 R,2R,4S)-bicyclo[2.2.1 ]heptan-2-ylamino)-2-oxoethyl)-2- oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(4-methyl-2- (trifluoromethyl)thiazole-5-carboxamido)-5-oxohexanediamide 11-130: (2S)-N1 -(1 -(2-((1 R,2R,4S)-bicyclo[2.2.1 ]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(1 -methyl-1 H-1,2,3-triazole-5-carboxam ido)-5-oxohexanediam ide 11-131: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)- N6-methyl-5-oxo-2-(2H-1,2,3-triazole-4-carboxamido)hexanediamide 11-132: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxo-2-(1 H-1,2,3-triazole-4-carboxamido)hexanediamide 11-133: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(1 -methyl-1 H-1,2,3-triazole-4-carboxamido)-5-oxohexanediamide 11-134: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxo-2-(1 H-1,2,4-triazole-3-carboxamido)hexanediamide 11-135: (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(1 -methyl-1 H-1,2,4-triazole-3-carboxamido)-5-oxohexanediamide 11-136: (S)-2-(benzofuran-3-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-137: (S)-2-(benzo[b]thiophene-3-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-138 (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(1-methyl-1 H-pyrazole-3-carboxamido)-5-oxohexanediamide 11-139 (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(1-methyl-1 H-pyrazole-4-carboxamido)-5-oxohexanediamide 11-140 (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(1-methyl-1 H-pyrazole-5-carboxamido)-5-oxohexanediamide 11-141 (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(4-methyl-1,2,3-thiadiazole-5-carboxamido)-5-oxohexanediamide 11-142 (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)- N6-methyl-5-oxo-2-(1,2,5-thiadiazole-3-carboxamido)hexanediamide 11-143 (S)-2-(4-iodo-1 -methyl-1 H-pyrazole-5-carboxamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-144 (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(1 -methyl-1 H-pyrazole-5-carboxamido)-5-oxohexanediamide 11-145 (S)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(4-methyl-1,2,3-thiadiazole-5-carboxamido)-5-oxohexanediamide 11-146 (S)-2-(benzofuran-2-carboxamido)-N1 -(1 -(2-((1 R,2R,4S)- bicyclo[2.2.1 ]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-d ihydropy rid in-3-yl)-5-oxohexanediamide 11-147 (S)-N1 -(1 -(2-((1 R,2R,4S)-bicyclo[2.2.1]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-148 (S)-2-(benzofuran-2-carboxamido)-N1 -(1 -(2-((1 S,2R,4R)- bicyclo[2.2.1 ]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide 11-149 (S)-N1 -(1 -(2-((1 S,2R, 4R)-bicyclo[2.2.1 ]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-150 (S)-2-(benzofuran-2-carboxamido)-5-oxo-N1-(2-oxo-1-(2-oxo-2-((1 R,2S,4R)-177-trimethylbicyclo[2.2.1]heptan-2-ylamino)ethyl)-1,2-dihydropyridin-3-yl)hexanediamide 11-151 (S)-2-(3-methylbenzofuran-2-carboxamido)-5-oxo-N1-(2-oxo-1-(2-oxo-2-((1 R,2S,4R)-1,7,7-trimethylbicyclo[2.2.1]heptan-2-ylamino)ethyl)-1,2-dihydropyridin-3-yl)hexanediamide 11-152 (S)-N1-(1-(2-((1 R,2R,4S)-bicyclo[2.2.1]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(4-methyl-1,2,3-thiadiazole-5-carboxam ido)-5-oxohexanediam ide 11-153 (S)-N1-(1-(2-((1 R,2R,4S)-bicyclo[2.2.1]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(1 -methyl-1 H-pyrazole-5-carboxamido)-5-oxohexanediam ide 11-154 (S)-N1 -(1 -(2-((1 S,2R, 4R)-bicyclo[2.2.1 ]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(4-methyl-2-(trifluoromethyl)thiazole-5-carboxam ido)-5-oxohexanediam ide 11-155 (S)-N1 -(1 -(2-((1 S,2R, 4R)-bicyclo[2.2.1 ]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(2,5-dichlorothiophene-3-carboxamido)-N6-methyl-5-oxohexanediam ide 11-156 (S)-N1 -(1 -(2-((1 S,2R, 4R)-bicyclo[2.2.1 ]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(4-methyl-1,2,3-thiadiazole-5-carboxam ido)-5-oxohexanediam ide 11-157 (S)-N1 -(1 -(2-((1 S,2R, 4R)-bicyclo[2.2.1 ]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(1 -methyl-1 H-1,2,3-triazole-5-carboxam ido)-5-oxohexanediam ide 11-158 (S)-N1 -(1 -(2-((1 S,2R, 4R)-bicyclo[2.2.1 ]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(1 -methyl-1 H-pyrazole-5-carboxamido)-5-oxohexanediam ide 11-159 (S)-N1-methyl-5-(4-methyl-2-(trifluoromethyl)thiazole-5-carboxamido)-2-oxo-N6-(2-oxo-1 -(2-oxo-2-((1 R,2S,4R)-1,7,7-trimethylbicyclo[2.2.1 ]heptan-2- ylamino)ethyl)-1,2-dihydropyridin-3-yl)hexanediamide 11-160 (8)-2-(2,5-dichlorothiophene-3-carboxamido)-N6-methyl-5-oxo-N1-(2-oxo-1-(2-oxo-2-((1 R,2S,4R)-1,7,7-trimethylbicyclo[2.2.1]heptan-2-ylamino)ethyl)-1,2-dihydropyridin-3-yl)hexanediamide 11-161 (S)-N1-methyl-5-(4-methyl-1,2,3-thiadiazole-5-carboxamido)-2-oxo-N6-(2-oxo-1 -(2-oxo-2-((1 R,2S,4R)-1,7,7-trimethylbicyclo[2.2.1 ]heptan-2-ylamino)ethyl)-1,2-dihydropyridin-3-yl)hexanediamide 11-162 (S)-N1-methyl-5-(1-methyl-1 H-1,2,3-triazole-5-carboxamido)-2-oxo-N6-(2-oxo-1 -(2-oxo-2-((1 R,2S,4R)-1,7,7-trimethylbicyclo[2.2.1 ]heptan-2-ylamino)ethyl)-1,2-dihydropyridin-3-yl)hexanediamide 11-163 (S)-N1-methyl-5-(1-methyl-1 H-pyrazole-5-carboxamido)-2-oxo-N6-(2-oxo-1-(2-oxo-2-((1 R,2S,4R)-1,7,7-trimethylbicyclo[2.2.1]heptan-2-ylamino)ethyl)-1,2-dihydropyridin-3-yl)hexanediamide 11-164 (2S)-2-(4-tert-butyl-1 H-pyrrole-3-carboxamido)-N6-methyl-N1 -(1 -(2-(1 -adamantylamino)ethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide 11-165 (2S)-2-(4-cyano-1-methyl-1 H-pyrrole-2-carboxamido)-N6-methyl-N1 -(1 -(3(1 -adamantylamino)propyl)-2-oxo-1,2-d ihydropyrid in-3-y l)-5-oxohexanediamide 11-166 (S)-N1 -(1 -(3-(2-adamantylamino)-3-oxopropyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(5-methoxyoxazole-2-carboxamido)-N6-methyl-5-oxohexanediamide 11-167 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-168 (S)-2-(2-acetyloxazole-4-carboxamido)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-169 (S)-N1 -(1 -(2-(bicyclo[2.1.1 ]hexan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-170 (S)-N1 -(1 -(2-(bicyclo[2.1.1 ]hexan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(2-isopropyloxazole-5-carboxamido)-N6-methyl-5-oxohexanediamide 11-171 (2S)-2-(benzofuran-2-carboxamido)-N1 -(1 -(2-(bicyclo[3.2.1 ]octan-8-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-172 (2S)-N1 -(1 -(2-(bicyclo[3.2.1 ]octan-8-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(3,5-dimethylisoxazole-4-carboxamido)-N6-methyl-5-oxohexanediamide 11-173 (S)-N1 -(1 -(2-(5-carboxy-2-aminoadamantane)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(4-methylpyrimidine-5-carboxamido)-5- oxohexanediamide 11-174 (2S)-N1 -(1 -(2-(4-aminoadamantane-N,N-dimethyl-1 -carboxamide)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxo-2-(1,2,3,4-tetrahydronaphthalene-2-carboxamido)hexanediamide 11-175 (S)-2-((S)-1,4-diazabicyclo[2.2.2]octane-2-carboxamido)-N6-tert-butyl-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide 11-176 (S)-N1-tert-butyl-5-(1 H-indole-3-carboxamido)-N6-(1-(2-(2-adamantylamino)- 2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-oxohexanediamide 11-177 (S)-N1 -tert-butyl-N6-(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(6-methylimidazo[2,1-b]thiazole-3-carboxamido)-2-oxohexanediamide 11-178 (S)-2-(benzo[d]thiazole-2-carboxamido)-N1-(1-(2-((1 S,2R,4R)-bicyclo[2.2.1 ]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-d ihydropy rid in-3-yl)- N6-cyclopentyl-5-oxohexanediamide 11-179 (S)-N1 -(1 -(2-((1 S,2R, 4R)-bicyclo[2.2.1 ]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-cyclopentyl-2-(imidazo[2,1-b]thiazole-6-carboxam ido)-5-oxohexanediam ide 11-180 (S)-N1 -(1 -(2-((1 S,2R, 4R)-bicyclo[2.2.1 ]heptan-2-ylamino)-2-oxoethyl)-2-oxo- 1,2-dihydropyridin-3-yl)-N6-cyclopentyl-2-(4-hydroxy-6- (trifluoromethoxy)quinoline-3-carboxamido)-5-oxohexanediamide 11-181 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(cinnoline-3-carboxamido)-N6-cyclohexyl-5-oxohexanediamide 11-182 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-cyclohexyl-2-(3-ethylbenzofuran-2-carboxamido)-5-oxohexanediamide 11-183 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-cyclohexyl-2-(1-ethyl-1 H-indole-2-carboxamido)-5-oxohexanediamide 11-184 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-cyclohexyl-2-(2-methyl-1,8-naphthyridine-3-carboxam ido)-5-oxohexanediam ide 11-185 (S)-N1 -(1 -(2-(bicyclo[2.1.1 ]hexan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxo-2-(1,2,3,4-tetrahydroquinoline-6-carboxam ido)hexanediam ide 11-186 (S)-N1-(1-(2-(2-carboxy-2-amino-5-(trifluoromethyl)adamantane)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxo-2-(3-oxo-1,2,3,4-tetrahydroisoquinoline-6-carboxamido)hexanediamide 11-187 (S)-N1 -(1 -(2-(5-ethyladamantane-2-amino)-2-oxoethyl)-2-oxo-1,2- dihydropyridin-3-yl)-N6-methyl-2-(1,6-naphthyridine-2-carboxamido)-5-oxohexanediamide 11-188 (S)-N1 -(1 -(2-(bicyclo[2.1.1 ]hexan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(2,6-naphthyridine-1-carboxamido)-5-oxohexanediamide 11-189 (S)-2-(4-amino-1,2,5-oxadiazole-3-carboxamido)-N1 -(1 -(2- (bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-d ihydropy rid in-3-y I)- N6-methyl-5-oxohexanediamide 11-190 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(6-(dimethylamino)benzofuran-2-carboxamido)-N6- methyl-5-oxohexanediamide 11-191 (S)-2-(2-acetamidothiazole-5-carboxamido)-N1-(1-(2-(bicyclo[1.1,1]pentan-1-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-192 (S)-N4-(1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-ylamino)-6-(methylamino)-1,5,6-trioxohexan-2-yl)-1 H-pyrrole-2,4-dicarboxamide 11-193 (S)-N1 -(1 -(2-(1 -acetylamino-4-aminoadamantane)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxo-2-(5-sulfamoylfuran-3-carboxam ido)hexanediam ide 11-194 (S)-2-(benzofuran-5-carboxam ido)-N 1 -(1 -(2-(1 -acetylam ino-4- aminoadamantane)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-195 (S)-2-(benzofuran-6-carboxamido)-N1 -(1 -(2-(4-aminoadamantane-1 -carboxamide)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide 11-196 (S)-N1-(1-(2-(4-aminoadamantane-1-carboxamide)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(3-(1-methylcyclopropyl)-1,2,4-oxadiazole-5-carboxamido)-5-oxohexanediamide 11-197 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(5-methyl-1,2,4-oxadiazole-3-carboxam ido)-5-oxohexanediam ide 11-198 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxo-2-(1,2,3-thiadiazole-4-carboxam ido)hexanediam ide 11-199 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxo-2-(1,2,4-thiadiazole-5-carboxam ido)hexanediam ide II-200 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxo-2-(1,3,4-thiadiazole-2- carboxam ido)hexanediam ide 11-201 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(4-cyclopropyl-1,2,3-thiadiazole-5-carboxamido)-N6- methyl-5-oxohexanediamide II-202 (S)-2-(4-cyclopropyl-1,2,3-thiadiazole-5-carboxamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-203 (S)-2-(4-isopropyl-1,2,3-thiadiazole-5-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-204 (S)-2-(4-ethyl-1,2,3-thiadiazole-5-carboxamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-205 (S)-2-(4-formyl-1,2,3-thiadiazole-5-carboxamido)-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-206 (S)-2-(4-(hydroxymethyl)-1,2,3-thiadiazole-5-carboxamido)-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-methyl-5-oxohexanediamide II-207 (S)-N 1 -(1 -(2-(1 -adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(1-methyl-1H-imidazole-5-carboxamido)-5-oxohexanediamide II-208 (S)-N 1-(1 -(2-(((1 S,2R,5S)-6,6-dimethylbicyclo[3.1.1]heptan-2-yl)methylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(1-methyl-1H-imidazole-2-carboxamido)-5-oxohexanediamide II-209 (S)-N 1-(1 -(2-(((1 R,2R,5R)-6,6-dimethylbicyclo[3.1.1]heptan-2-yl)methylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(1H-imidazole-4-carboxamido)-N6-methyl-5-oxohexanediamide 11-210 (S)-N 1-(1 -(2-(3,5-dimethyladamantane-1-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(1-methyl-1H-imidazole-5-carboxamido)-5-oxohexanediamide 11-211 (S)-N 1-(1 -(2-(3,5,7-trimethyl-1-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-methyl-2-(1-methyl-1H-imidazole-5-carboxamido)-5-oxohexanediamide or a pharmaceutically acceptable salt thereof. In some other preferred embodiments, the reversible TG2 inhibitor is a compound of the general formula (lrev) selected from the group consisting of: Compound Name 1-1: (S)-N1 -ethyl-N6-(1 -(2-(1 -adamantylamino)-2-oxoethyl)-2-oxo-1,2- dihydropyridin-3-yl)-5-(1-methyl-1 H-imidazole-5-carboxamido)-2-oxohexanediamide, I-2: (S)-N1 -ethy 1-5-( 1 H-imidazole-4-carboxamido)-N6-(1 -(2-(1 -adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-oxohexanediamide, I-3: (S)-N1 -ethyl-N6-(1 -(2-(1 -adamantyl(methyl)amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1-methyl-1 H-imidazole-5-carboxamido)-2-oxohexanediamide, I-4: (S)-N1 -ethyl-N6-(1 -(2-(3,5-dimethyladamantane-1 -amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1 -methyl-1 H-imidazole-5-carboxamido)-2-oxohexanediamide, I-5: (S)-N1 -ethyl-N6-(1 -(2-(3-ethyladamantane-1 -amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1-methyl-1 H-imidazole-5-carboxamido)-2-oxohexanediamide, I-6: (S)-N1-ethyl-N6-(1-(2-(3-trifluoromethyladamantane-1-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1 -methyl-1 H-imidazole-5-carboxamido)-2-oxohexanediamide, I-7: (S)-N1 -ethyl-N6-(1 -(2-(3-hydroxyadamantane-1 -amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1 -methyl-1 H-imidazole-5-carboxamido)-2-oxohexanediamide, I-8: (S)-N1 -ethyl-N6-(1 -(2-(3-fluoroadamantane-1 -amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1-methyl-1 H-imidazole-5-carboxamido)-2-oxohexanediamide, I-9: (S)-N1-ethyl-N6-(1-(2-(3-chloroadamantane-1-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1-methyl-1 H-imidazole-5-carboxamido)-2-oxohexanediamide, 1-10: (S)-N1-ethyl-N6-(1-(2-(3-bromoadamantane-1-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1-methyl-1 H-imidazole-5-carboxamido)-2-oxohexanediamide, 1-11: (S)-N1-ethyl-N6-(1-(2-(3-methyl     adamantane-3-carboxylate-1-amino)-2- oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1 -methyl-1 H-imidazole-5-carboxam ido)-2-oxohexanediam ide, 1-12: (S)-N1 -ethy l-N6-( 1 -(2-(4,4-difluoroadamantane-1 -amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1 -methyl-1 H-imidazole-5-carboxamido)-2-oxohexanediamide, 1-13: (S)-N1-(1-(2-(((1S,2R,5S)-6,6-dimethylbicyclo[3.1.1]heptan-2- yl)methylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-2-(1 -methyl-1 H-imidazole-5-carboxamido)-5-oxohexanediamide, 1-14: (S)-N1-(1-(2-(((1R,2R,5R)-6,6-dimethylbicyclo[3.1.1]heptan-2- yl)methylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-2-(1 -methyl-1 H-imidazole-5-carboxamido)-5-oxohexanediamide, 1-15: (S)-N1 -ethyl-N6-(1 -(2-(3-ethyladamantane-1 -amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1-methyl-1 H-imidazole-4-carboxamido)-2-oxohexanediamide, 1-16: (S)-N1 -ethyl-N6-(1 -(2-(3-ethyladamantane-1 -amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1-methyl-1 H-imidazole-2-carboxamido)-2-oxohexanediamide, 1-17: (8)-2-(1,4-dimethyl-1 H-imidazole-5-carboxamido)-N6-ethyl-N1 -(1 -(2-(3-ethyladamantane-1-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, 1-18: (S)-N1 -ethy 1-5-( 1 -isobutyl-1 H-imidazole-4-carboxamido)-N6-(1 -(2-(3-ethyladamantane-1-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-oxohexanediamide, 1-19: (S)-2-(1 -cyclopentyl-1 H-imidazole-4-carboxamido)-N6-ethyl-N1 -(1 -(2-(3-ethyladamantane-1-amino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-20: (S)-2-(1-cyclobutyl-1 H-imidazole-4-carboxamido)-N6-ethyl-N1 -(1 -(2-(3-ethyladamantane-1-amino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, 1-21: (S)-2-(1,4-dimethyl-1 H-imidazole-5-carboxamido)-N6-ethyl-N1-(1-(2-(3,5-dimethyladamantane-1-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-22: (S)-N1 -ethyl-N6-(1 -(2-(3,5-dimethyladamantane-1 -amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1 -methyl-1 H-imidazole-4-carboxamido)-2-oxohexanediamide, I-23: (S)-N1 -ethyl-N6-(1 -(2-(3,5-dimethyladamantane-1 -amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1 -methyl-1 H-imidazole-2-carboxamido)-2-oxohexanediamide, I-24: (S)-2-(1,2-dimethyl-1 H-imidazole-5-carboxamido)-N6-ethyl-N1 -(1 -(2-(3,5-dimethyladamantane-1-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-25: (S)-N1-ethyl-N6-(1-(2-(3-methyladamantane-1-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1 -methyl-1 H-imidazole-5-carboxamido)-2-oxohexanediamide, I-26: (S)-2-(2-chloro-1 -methyl-1 H-imidazole-5-carboxamido)-N6-ethyl-N1 -(1 -(2-(3,5-dimethyladamantane-1-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-27: (S)-2-(1,2-dimethyl-1 H-imidazole-5-carboxamido)-N6-ethyl-N1 -(1 -(2-(3-methyladamantane-1-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-28: (S)-N1-ethyl-N6-(1 -(2-(3,5,7-trimethyl-1-adamantylamino)-2-oxoethyl)-2-oxo- 1,2-d ihydropy rid in-3-y 1)-5-( 1 -methyl-1 H-imidazole-5-carboxamido)-2-oxohexanediamide, I-29: (S)-2-(2-chloro-1 -methyl-1 H-imidazole-5-carboxamido)-N6-ethyl-N1 -(1 -(2-(3,5,7-trimethyl-1-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-30 (S)-2-(benzofuran-2-carboxamido)-N6-ethyl-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, 1-31 (S)-N1 -ethyl-N6-(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(3-methylbenzofuran-2-carboxamido)-2-oxohexanediamide, I-32 (S)-2-(3-chlorobenzofuran-2-carboxamido)-N6-ethyl-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-33 (S)-2-(4-bromobenzofuran-2-carboxamido)-N6-ethyl-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-34 (S)-2-(benzo[b]thiophene-2-carboxamido)-N6-ethyl-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-35 (S)-N1 -ethyl-5-(7-fluorobenzo[b]thiophene-2-carboxamido)-N6-(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-2-oxohexanediamide, I-36 (S)-2-(4,5-difluoro-1 H-indole-2-carboxamido)-N6-ethyl-N 1-( 1-(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-37 (S)-N1 -ethyl-N6-(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(3-methyl-1 H-indole-2-carboxamido)-2-oxohexanediamide, I-38 (8)-2-(1 H-benzo[d]imidazole-2-carboxamido)-N6-ethyl-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-39 (S)-2-(2,3-dihydro-1 H-indene-2-carboxamido)-N6-ethyl-N 1-( 1-(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-40 (S)-N1 -ethyl-N6-(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2- dihydropyridin-3-yl)-5-(4-methyl-2-(trifluoromethyl)thiazole-5-carboxamido)-2-oxohexanediam ide, 1-41 (S)-2-(4-bromo-2-(trifluoromethyl)thiazole-5-carboxamido)-N6-ethyl-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-42 (S)-N1 -ethyl-N6-(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(4-methyl-2-phenylthiazole-5-carboxamido)-2-oxohexanediamide, I-43 (S)-2-(5-bromo-3-methylthiophene-2-carboxamido)-N6-ethyl-N 1-(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-44 (8)-2-(3,5-dibromothiophene-2-carboxamido)-N6-ethyl-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-45 (S)-2-(5-bromo-3-methylfuran-2-carboxamido)-N6-ethyl-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-46 (S)-2-(2,5-dichlorothiophene-3-carboxamido)-N6-ethyl-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-47 (S)-2-(2,5-dibromothiophene-3-carboxamido)-N6-ethyl-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-48 (S)-2-(2,5-dichlorothiazole-4-carboxamido)-N6-ethyl-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-49 (S)-2-(2,5-dimethylfuran-3-carboxamido)-N6-ethyl-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-50 (S)-2-(4-bromothiazole-2-carboxamido)-N6-ethyl-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, 1-51 (S)-2-(4-bromothiophene-2-carboxamido)-N6-ethyl-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-52 (S)-2-(4-bromo-5-chlorothiophene-2-carboxamido)-N6-ethyl-N 1-(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-53 (S)-2-(4,5-dibromothiophene-2-carboxamido)-N6-ethyl-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5- oxohexanediamide, I-54 (8)-2-(4,5-dichlorothiophene-2-carboxamido)-N6-ethyl-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-55 (S)-2-((S)-1-acetylpyrrolidine-2-carboxamido)-N6-ethyl-N1 -(1 -(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-56 (S)-N1 -ethyl-N6-(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1 -methyl-1 H-1,2,3-triazole-5-carboxamido)-2-oxohexanediamide, I-57 (S)-N1 -ethyl-N6-(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-oxo-5-(2H-tetrazole-5-carboxamido)hexanediamide, I-58 (S)-N1-ethyl-N6-(1-(2-(5-hydroxyadamantane-2-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-oxo-5-(pyrazine-2-carboxamido)hexanediamide, I-59 (S)-N1 -ethyl-N6-(1 -(2-(5-fluoroadamantane-2-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-oxo-5-((S)-pyrrolidine-3-carboxamido)hexanediamide, I-60 (S)-N1 -ethyl-N6-(1 -(2-(5-chloroadamantane-2-amino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-2-oxo-5-((S)-piperidine-2-carboxamido)hexanediamide, 1-61 (S)-N1 -ethyl-N6-(1 -(2-(5-bromoadamantane-2-amino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-2-oxo-5-((R)-piperidine-3-carboxamido)hexanediamide, I-62 (S)-N1-ethyl-N6-(1-(2-(5-methyladamantane-2-amino)-2-oxoethyl)-2-oxo- 1,2-dihydropyridin-3-yl)-5-((R)-morpholine-3-carboxamido)-2-oxohexanediamide, I-63 (S)-N1-ethyl-N6-(1-(2-(2-carbonitrileadamantane-2-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-oxo-5-((3S,4R)-quinuclidine-3- carboxam ido)hexanediam ide, I-64 (S)-methyl 3-(6-(ethylamino)-1 -(1 -(2-(methyl 2-aminoadamantane-2-carboxylate)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-ylamino)-1,5,6-trioxohexan-2-ylcarbamoyl)-5-nitrobenzoate, I-65 (S)-N1 -(1 -(2-(1 -adamantylmethylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-2-(5-nitronicotinamido)-5-oxohexanediamide, I-66 5-((28)-1 -(1-(2-1 -adamantylmethylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-ylamino)-6-(ethylamino)-1,5,6-trioxohexan-2-ylcarbamoyl)nicotinic acid, I-67 (S)-N1 -ethyl-N6-(1 -(2-(2-adamantyl(methyl)amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(6-methylimidazo[2,1-b]thiazole-5-carboxamido)-2-oxohexanediamide, I-68 (S)-N1 -(1 -(2-((1 S, 2R,4R)-bicyclo[2.2.1]heptan-2-ylamino)-2-oxoethyl)-2-oxo- 1,2-dihydropyridin-3-yl)-N6-ethyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide, I-69 (S)-N1-ethyl-5-(3-methylbenzofuran-2-carboxamido)-2-oxo-N6-(2-oxo-1-(2-oxo-2-((1 R,2S,4R)-1,7,7-trimethylbicyclo[2.2.1 ]heptan-2-ylamino)ethyl)-1,2-dihydropyridin-3-yl)hexanediamide, I-70 (S)-N1 -(1 -(2-((1 R,2R,4S)-bicyclo[2.2.1]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide, 1-71 (S)-N1 -(1 -(2-((1 s,4R)-bicyclo[2.2.1 ]heptan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-2-(isonicotinamido)-5-oxohexanediamide, I-72 (S)-N1 -(1 -(2-(bicyclo[2.2.1 ]heptan-7-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-5-oxo-2-(pyridazine-4- carboxam ido)hexanediam ide, I-73 (S)-N1 -(1 -(2-((1 R,2R,4R)-bicyclo[2.2.1]hept-5-en-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-5-oxo-2-(pyridazine-3- carboxam ido)hexanediam ide, I-74 (2S)-N1 -(1 -(2-(bicyclo[2.2.2]octan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-5-oxo-2-(2H-1,2,3-triazole-4-carboxam ido)hexanediam ide, I-75 (S)-N1 -ethy 1-5-( 1 -methyl-1 H-1,2,3-triazole-4-carboxamido)-2-oxo-N6-(2-oxo-1 -(2-oxo-2-((1 R,2R,4R)-1,7,7-trimethylbicyclo[2.2.1 ]heptan-2-ylamino)ethyl)-1,2-dihydropyridin-3-yl)hexanediamide, I-76 (S)-N1 -ethyl-5-(1 -methyl-1 H-1,2,4-triazole-3-carboxamido)-2-oxo-N6-(2-oxo-1 -(2-oxo-2-((1 R,2R,3R,5S)-2,6,6-trimethylbicyclo[3.1.1 ]heptan-3-ylamino)ethyl)-1,2-dihydropyridin-3-yl)hexanediamide, I-77 (S)-2-(benzofuran-3-carboxam ido)-N6-ethyl-5-oxo-N 1 -(2-oxo-1 -(2-oxo-2-((1 S,2S,3S,5R)-2,6,6-trimethylbicyclo[3.1.1 ]heptan-3-ylamino)ethyl)-1,2-dihydropyridin-3-yl)hexanediamide, I-78 (S)-2-(benzo[b]thiophene-3-carboxamido)-N6-ethyl-N1 -(1 -(2-(4-homoisotwistane-3-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-79 (S)-N1 -ethyl-N6-(1 -(2-(diamantane-1 -amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1-methyl-1 H-pyrazole-4-carboxamido)-2-oxohexanediamide, I-80 (S)-N1 -ethyl-N6-(1 -(2-(diamantane-4-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1-methyl-1 H-pyrazole-3-carboxamido)-2-oxohexanediamide, 1-81 (S)-N1 -(1 -(1 -adamantylmethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-2-(1- methyl-1 H-pyrazole-5-carboxamido)-5-oxohexanediamide, I-82 (S)-N1 -(1 -((3-hydroxy-1 -adamantyl)methyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(4-cyclopropyl-1,2,3-thiadiazole-5-carboxamido)-N6-ethyl-5-oxohexanediamide, I-83 (S)-N1-(1-((3-bromo-1-adamantyl)methyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-5-oxo-2-(1,2,5-thiadiazole-3-carboxamido)hexanediamide, I-84 (S)-N1 -(1 -(2-adamantylmethyl)-2 -oxo-1,2-d ihydropyridin-3-yl)-N6-ethy 1-2-(4-(hydroxymethyl)-l ,2,3-thiadiazole-5-carboxamido)-5-oxohexanediamide, I-85 (S)-2-(4-tert-butyl-1 H-pyrrole-3-carboxamido)-N1 -(1 -(2-(1 -adamantylamino)ethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-5-oxohexanediamide, I-86 (S)-2-(4-cyano-1 -methyl-1 H-pyrrole-2-carboxamido)-N1 -(1 -(1 -adamantylamino)propyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-5-oxohexanediamide, I-87 (S)-N1 -(1 -(3-(2-adamantylamino)-3-oxopropyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-2-(5-methoxyoxazole-2-carboxamido)-5-oxohexanediamide, I-88 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-2-(3-methylbenzofuran-2-carboxamido)-5-oxohexanediamide, I-89 (S)-2-(2-acetyloxazole-4-carboxamido)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-5-oxohexanediamide, I-90 (S)-N1 -(1 -(2-(bicyclo[2.1.1 ]hexan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-2-(2-isopropyloxazole-5-carboxamido)-5-oxohexanediamide, 1-91 (2S)-N1 -(1 -(2-(bicyclo[3.2.1 ]octan-8-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(3,5-dimethylisoxazole-4-carboxamido)-N6-ethyl-5-oxohexanediamide, I-92 (S)-N1-ethyl-N6-(1-(2-(5-carboxy-2-aminoadamantane)-2-oxoethyl)-2-oxo- 1,2-dihydropyridin-3-yl)-5-(4-methylpyrimidine-5-carboxamido)-2-oxohexanediamide, I-93 (5S)-N1 -ethyl-N6-(1 -(2-(4-aminoadamantane-N,N-dimethyl-1 -carboxamide)- 2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-oxo-5-(1,2,3,4- tetrahydronaphthalene-2-carboxamido)hexanediamide, I-94 (S)-2-((S)-1,4-diazabicyclo[2.2.2]octane-2-carboxamido)-N6-ethyl-N1-(1-(2-(2-adamantylamino)-2-oxoethyl)-2 -oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, I-95 (S)-N1 -ethyl-5-(1 H-indole-3-carboxamido)-N6-(1 -(2-(2-adamantylamino)-2- oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2 -oxohexanediamide, I-96 (S)-N1 -ethyl-N6-(1 -(2-(2-adamantylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(6-methylimidazo[2,1-b]thiazole-3-carboxamido)-2-oxohexanediamide, I-97 (S)-2-(benzo[d]thiazole-2-carboxamido)-N1-(1-(2-((1 S,2R,4R)- bicyclo[2.2.1 ]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1, 2-d ihydropy rid in-3-yl)-N6-ethyl-5-oxohexanediam ide, I-98 (S)-N1 -(1 -(2-((1 S,2R, 4R)-bicyclo[2.2.1 ]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-2-(imidazo[2,1-b]thiazole-6-carboxamido)-5-oxohexanediam ide, I-99 (S)-N1 -(1 -(2-((1 S,2R, 4R)-bicyclo[2.2.1 ]heptan-2-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-2-(4-hydroxy-6-(trifluoromethoxy)quinoline-3-carboxamido)-5-oxohexanediamide, 1-100 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(cinnoline-3-carboxamido)-N6-ethyl-5-oxohexanediamide, 1-101 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-2-(3-ethylbenzofuran-2-carboxamido)-5-oxohexanediamide, 1-102 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-2-(1 -ethyl-1 H-indole-2-carboxamido)-5-oxohexanediamide, 1-103 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-2-(2-methyl-1,8-naphthyridine-3-carboxamido)-5-oxohexanediam ide, 1-104 (S)-N1 -(1 -(2-(bicyclo[2.1.1 ]hexan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-5-oxo-2-(1,2,3,4-tetrahydroquinoline-6-carboxam ido)hexanediam ide, 1-105 (S)-N1-ethyl-N6-(1-(2-(2-carboxy-2-amino-5-(trifluoromethyl)adamantane)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-oxo-5-(3-oxo-1,2,3,4-tetrahydroisoquinoline-6-carboxamido)hexanediamide, 1-106 (S)-N1 -ethyl-N6-(1 -(2-(5-ethyladamantane-2-amino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(1,6-naphthyridine-2-carboxamido)-2-oxohexanediamide, 1-107 (S)-N1 -(1 -(2-(bicyclo[2.1.1 ]hexan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-2-(2,6-naphthyridine-1-carboxamido)-5-oxohexanediamide, 1-108 (S)-2-(4-amino-1,2,5-oxadiazole-3-carboxamido)-N1-(1-(2- (bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1, 2-d ihydropy rid in-3-y I)- N6-ethyl-5-oxohexanediam ide, 1-109 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-(6-(dimethylamino)benzofuran-2-carboxamido)-N6-ethyl-5-oxohexanediamide, 1-110 (S)-2-(2-acetamidothiazole-5-carboxamido)-N1-(1-(2-(bicyclo[1.1,1]pentan-1-ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-5-oxohexanediamide, 1-111 (S)-N4-(1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-ylamino)-6-(ethylamino)-1,5,6-trioxohexan-2-yl)-1 H-pyrrole-2,4-dicarboxamide, 1-112 (S)-N1 -ethyl-N6-(1 -(2-(1 -acetylamino-4-aminoadamantane)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-2-oxo-5-(5-sulfamoylfuran-3- carboxam ido)hexanediam ide, 1-113 (S)-2-(benzofuran-5-carboxamido)-N6-ethyl-N1 -(1 -(2-(1 -acetylamino-4-aminoadamantane)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-oxohexanediamide, 1-114 (S)-2-(benzofuran-6-carboxamido)-N6-ethyl-N1-(1-(2-(4-aminoadamantane- 1 -carboxamide)-2-oxoethyl)-2-oxo-1,2-d ihydropyrid in-3-y l)-5-oxohexanediamide, 1-115 (S)-N1-ethyl-N6-(1-(2-(4-aminoadamantane-1-carboxamide)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-5-(3-(1 -methylcyclopropyl)-1,2,4-oxadiazole-5-carboxam ido)-2-oxohexanediam ide, 1-116 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-2-(5-methyl-1,2,4-oxadiazole-3-carboxamido)-5-oxohexanediam ide, 1-117 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-5-oxo-2-(1,2,3-thiadiazole-4-carboxam ido)hexanediam ide, 1-118 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-5-oxo-2-(1,2,4-thiadiazole-5-carboxam ido)hexanediam ide, 1-119 (S)-N1 -(1 -(2-(bicyclo[1.1.1 ]pentan-1 -ylamino)-2-oxoethyl)-2-oxo-1,2-dihydropyridin-3-yl)-N6-ethyl-5-oxo-2-(1,3,4-thiadiazole-2-carboxam ido)hexanediam ide, 1-120 (S)-N1-ethyl-5-(4-formyl-1,2,3-thiadiazole-5-carboxamido)-N6-(1-(2-(2-adaman...

Claims

1. A computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of at least one transglutaminase 2 inhibitor in the treatment of celiac disease of said subject, the method comprising:(a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject;(b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to(i) a first gluten-sensitive DQ genotype group,(ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger gluten-specific T-cell response than the second gluten-sensitive DQ genotype group, wherein the second gluten-sensitive DQ genotype group has a stronger gluten-specific T cell response than the third gluten-sensitive DQ genotype group,wherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to mature enterocytes and / or cell proliferation and / or inflammation; and(c) selecting or adjusting a therapy regimen for said subject based on the DQ genotype group (i), (ii), or (iii) of said subject,wherein the therapy regimen comprises one or more therapeutic measures selected from a dose level of transglutaminase 2 inhibitor, an administration interval of transglutaminase 2 inhibitor, type of transglutaminase 2 inhibitor, and duration of treatment, wherein one or more of the therapeutic measures vary depending on whether said subject applying to DQ genotype group (i), (ii), or (iii), and wherein selecting or adjusting a therapy regimen for said subject comprises selecting or adjusting one or more of the therapeutic measures based on the DQ genotype group of said subjectwherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, and preferablywherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of:HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; andwherein the HLA-DQ8 haplotypes are selected from the group comprising or consisting of:HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 I one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO.

2. The computer-implemented method according to claim 1, wherein before step (a) the method further comprises steps (a’) and (a”):(a’) obtaining an ex-vivo sample of genetic material from said subject;(a”) determining the human leukocyte antigen class II genotype of said subject in said ex-vivo sample of genetic material,wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject.

3. The computer-implemented method according to claim 1 or 2, wherein for a subject applying to the first gluten-sensitive DQ genotype group (i) the therapeutic regimen comprises one or more of administering the TG2 inhibitor at a higher dose, administering the TG2 inhibitor at higher frequency, longer duration of treatment, administering a more potent TG2 inhibitor than a therapeutic regimen for a subject applying to the second gluten-sensitive DQ genotype group (ii) or third gluten-sensitive DQ genotype group (iii).

4. The method according to any one of the claims 1 - 3, wherein the human leukocyte antigen DQ haplotypes include at least HLA-DQ2 and HLA-DQ8 haplotypes, andwherein the HLA-DQ2 haplotypes are selected from the group comprising or consisting of:HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; andwherein the HLA-DQ8 haplotypes are selected from the group comprising or consisting of:HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 half heterodimer, DQ2.5 I one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO.

5. The computer-implemented method according to any one of the claims 1 - 4, wherein step (b) further comprises:identifying said subject as applying to first gluten-sensitive DQ genotype group (i) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.5 I DQ2.5, DQ2.5 I DQ2.3, DQ2.5 I one copy of DQB1 *02, oridentifying said subject as applying to second gluten-sensitive DQ genotype group (ii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.2 HOMO, DQ8 HOMO, DQ8 / DQ2, DQ2.5 / DQ2.2, oridentifying said subject as applying to third gluten-sensitive DQ genotype group (iii) if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2 half heterodimer, DQ2.2 HETERO, DQ2.5 HETERO, DQ2.5 TrHETERO, DQ8 HETERO, DQ2.5 / one copy of DQA1*05.

6. The computer-implemented method according to any one of the claims 1 - 5, wherein a subject applying to the first gluten-sensitive DQ genotype group is characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.7 to -3.0, preferably between -1.0 to -2.7 from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet.

7. The computer-implemented method according to any one of the claims 1 - 6, wherein a subject applying to the second gluten-sensitive DQ genotype group is characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.1 to -1.3, between -0.4 to -1.0 from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet.

8. The computer-implemented method according to any one of the claims 1 - 7, wherein a subject applying to the third gluten-sensitive DQ genotype group is characterized by a change in villous height to crypt depth (VH:CrD) ratio10.between -0.05 to -0.7, preferably between -0.1 to -0.4 from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet.The computer-implemented method according to any one of the claims 1 - 8, wherein step b) comprises:(b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as applying to (i) a first gluten-sensitive DQ genotype group, (ii) a second gluten-sensitive DQ genotype group, or (iii) a third gluten-sensitive DQ genotype group, wherein the first gluten-sensitive DQ genotype group has a stronger gluten-specific T-cell response than the second gluten-sensitive DQ genotype group characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.7 to -3.0, preferably between -1.0 to -2.7 from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet;wherein the second gluten-sensitive DQ genotype group has a stronger gluten-specific T cell response than the third gluten-sensitive DQ genotype group characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.1 to -1.3, between -0.4 to -1.0 from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet;wherein third gluten-sensitive DQ genotype group has a gluten-specific T cell response characterized by a change in villous height to crypt depth (VH:CrD) ratio between -0.05 to -0.7, preferably between -0.1 to -0.4 from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free dietwherein stronger gluten-specific T-cell response is characterized by a more dysregulated genexpression of genes related to mature enterocytes and / or cell proliferation and / or inflammation.The computer-implemented method according to any one of the claims 1 - 9, wherein the first gluten-sensitive DQ genotype group has a more dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein more dysregulated genexpression is characterized byat least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 are at least 50% more downregulated in the first glutensensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% - 90%; and / orat least one, preferably more than one of the genes AGR2, MKI167, and CENPF are at least 30% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 33 -100%; and / orat least one, preferably more than one of the genes STAT1, GBP1 and TGM2 are at least 50% more upregulated in the first gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 50% - 100%.

11. The computer-implemented method according to any one of the claims 1-10, wherein the second gluten-sensitive DQ genotype group has a more dysregulated genexpression than the third gluten-sensitive DQ genotype group, wherein more dysregulated genexpression is characterized byat least one, preferably more than one of the genes APOB, APOA1, and TM4SF4 are are between 10% - 49% more downregulated in the second gluten-sensitive DQ genotype group than in the third glutensensitive DQ genotype group; and / orat least one, preferably more than one of the genes AGR2, MKI167, and CENPF are between 10% - 29% more upregulated in the second gluten-sensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 12% - 25%; and / orat least one, preferably more than one of the genes STAT1, GBP1 and TGM2 are between 1% - 49% more upregulated in the second glutensensitive DQ genotype group than in the third gluten-sensitive DQ genotype group, preferably between 5% - 20%.

12. The computer-implemented method according to any one of the claims 1 - 11, wherein the first gluten-sensitive DQ genotype group has a more dysregulated group of genes of a biological pathway than the third glutensensitive DQ genotype group, wherein a more dysregulated group of genes of a biological pathway is characterized byfor transit amplifying cells, genes from the first gluten-sensitive DQ genotype group are on average at least 50% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / orfor mature enterocytes genes from the first gluten-sensitive DQ genotype group are on average at least 200% more downregulated than genes from the third gluten-sensitive DQ genotype group, and / orfor immune cells, genes from the first gluten-sensitive DQ genotype group are on average at least 100% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / orfor duodenal transporter cells, genes from the first gluten-sensitive DQ genotype group are on average at least 200% more upregulated than genes from the third gluten-sensitive DQ genotype group.

13. The computer-implemented method according to any one of the claims 1-12, wherein the second gluten-sensitive DQ genotype group has a more dysregulated group of genes of a biological pathway than the third glutensensitive DQ genotype group, wherein a more dysregulated group of genes of a biological pathway is characterized byfor transit amplifying cells, genes from the second gluten-sensitive DQ genotype group are on average at least 20% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / orfor mature enterocytes, genes from the second gluten-sensitive DQ genotype group are on average at least 50% more downregulated than genes from the third gluten-sensitive DQ genotype group, and / orfor immune cells, genes from the second gluten-sensitive DQ genotype group are on average at least 5% more upregulated than genes from the third gluten-sensitive DQ genotype group, and / orfor duodenal transporter cells, genes from the second glutensensitive DQ genotype group are on average at least 50% more upregulated than genes from the third gluten-sensitive DQ genotype group.

14. The computer-implemented method according to any one of the claims 1-13, wherein the therapy regimen comprises TG2 inhibitor at a daily dose between 0.1 mg - 1000 mg, preferably between 0.5 mg - 500 mg, more preferably between 25 mg - 250 mg, most preferably between 1 mg - 100 mg.

15. The computer-implemented method according to any one of the claims 1-14, wherein the therapy regimen comprises TG2 inhibitor at a daily dose between 150 mg - 250 mg, more preferably between 160 mg - 240 mg,more preferably between 170 mg - 230 mg, more preferably between 180 mg - 220 mg, more preferably between 190 mg - 210 mg, preferably for the first gluten-sensitive DQ genotype.

16. The computer-implemented method according to any one of the claims 1-15, wherein the therapy regimen for the first gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 25 mg -1000 mg, preferably between 25 mg - 500 mg, more preferably between 25 mg - 250 mg, most preferably between 30 mg - 100 mg, and / or wherein the therapy regimen for the second gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 5 mg - 750 mg, more preferably between 5 mg - 250 mg, preferably between 5 mg - 75 mg, most preferably between 10 mg - 30 mg, and / orwherein the therapy regimen for the third gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 0.1 mg - 500 mg, more preferably between 0.1 mg - 250 mg, preferably between 0.1 mg - 50 mg, most preferably between 1 mg - 10 mg.

17. The computer-implemented method according to any one of the claims 1-16, wherein the therapy regimen for the first gluten-sensitive DQ genotype group comprises TG2 inhibitor at a daily dose between 150 mg -250 mg, more preferably between 160 mg - 240 mg, more preferably between 170 mg - 230 mg, more preferably between 180 mg - 220 mg, more preferably between 190 mg - 210 mg most preferably at a daily dose of (about) 200 mg.

18. The computer-implemented method according to any one of the claims 1-17, wherein step b) further comprisesidentifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as a subject having a risk for refractory coeliac disease or as a subject suffering from refractory coeliac disease; and applying said subject to the first gluten-sensitive DQ genotype group.

19. A computer-implemented method for selecting a therapy regimen for a subject having been diagnosed with celiac disease, wherein the therapy regimen comprises at least the use of a therapeutically effective amount of atleast one transglutaminase 2 inhibitor in the treatment of the celiac disease of said subject, the method comprising:(a) providing a human leukocyte antigen class II genotype of said subject, wherein the human leukocyte antigen class II genotype comprise human leukocyte antigen DQ haplotypes of said subject;(b) identifying said subject, at least based on the determined human leukocyte antigen DQ haplotypes of said subject, as a subject having a risk for refractory coeliac disease or as a subject suffering from refractory coeliac disease;(c) selecting or adjusting a therapy regimen for said subject if the subject has been identified having a risk for refractory coeliac diseases or suffering from refractory coeliac diseases ,wherein the therapy regimen comprises one or more therapeutic measures selected from dose level of TG2 inhibitor, administration interval of TG2 inhibitor, type of TG2 inhibitor, and duration of treatment.

20. The computer-implemented method according to claim 19, wherein before step (a) the method further comprises steps (a’) and (a”):(a’) obtaining an ex-vivo sample of genetic material from said subject;(a”) determining the human leukocyte antigen class II genotype of said subject in said ex-vivo sample of genetic material,wherein the human leukocyte antigen class II genotype comprises one or more of human leukocyte antigen DQ alleles and haplotypes of said subject.

21. The computer-implemented method according to Claims 19 or 20, wherein the human leukocyte antigen DQ haplotypes include one or more of HLA-DQ2, HLA-DQ3, HLA-DQ4, HLA-DQ5, HLA-DQ6, HLA-DQ7, HLA-DQ8, and HLA-DQ9 haplotypes, preferably HLA-DQ2 and HLA-DQ8 haplotypes, and preferably, wherein the HLA-DQ2 haplotypes are selected from the group consisting of: HLA-DQ2.2 / HLA-DQ2.2, HLA-DQ2.3 / HLA-DQ2.3, HLA-DQ2.5 / HLA-DQ2.5; HLA-DQ2.2 homodimer, HLA-DQ2.3 homodimer, HLA-DQ2.5 homodimer; HLA-DQ2.2 heterodimer, HLA-DQ2.3 heterodimer, HLA-DQ2.5 heterodimer; andwherein the HLA-DQ8 haplotypes are selected from the group consisting of: HLA-DQ8 homodimer, HLA-DQ8 heterodimer, DQ2.5 I one copy of DQB1*02, DQ2.5 / DQ2.3, DQ2.5 / DQ2.2, DQ8 / DQ2, DQ2 halfheterodimer, DQ2.5 I one copy of DQA1*05, DQ2 half heterodimer, and DQ2.5 TrHETERO.

22. The computer-implemented method according to any one of the claims 19 - 21, wherein step (b) further comprises:identifying said subject as a as a subject having a risk for refractory coeliac disease or as a subject suffering from refractory coeliac disease if the HLA-DQ2 and HLA-DQ8 haplotypes are DQ2.5 I DQ2.5, DQ2.5 I DQ2.3, DQ2.5 I one copy of DQB1*02.

23. The computer-implemented method according to any one of the claims 19-22, wherein a subject having a risk for refractory coeliac disease or a subject suffering from refractory coeliac disease is characterized by a change of villous height to crypt depth (VH:CrD) ratio between -1.0 to -2.7 (-1.0 > VH:CrD ratio > -2.7) from a villous height to crypt depth (VH:CrD) ratio of a comparative subject on gluten-free diet.

24. The computer-implemented method according to any one of the claims 19-23, wherein for a subject having a risk for refractory coeliac disease or suffering from refractory coeliac disease the therapeutic regimen comprises one or more of administering the TG2 inhibitor at a higher dose, administering the TG2 inhibitor at higher frequency, longer duration of treatment, administering a more potent TG2 inhibitor than a therapeutic regimen for a subject not suffering from refractory coeliac disease.

25. The computer-implemented method according to any one of the claims 19-24, wherein the therapy regimen comprises TG2 inhibitor at a daily dose between 25 mg - 1000 mg, more preferably between 25 mg - 250 mg, preferably between 25 mg - 500 mg, most preferably between 30 mg - 100 mg.

26. The computer-implemented method according to any one of the claims 19-25, wherein the therapy regimen preferably comprises TG2 inhibitor at a daily dose between 150 mg - 250 mg, more preferably between 160 mg -240 mg, more preferably between 170 mg - 230 mg, more preferably between 180 mg - 220 mg, more preferably between 190 mg - 210 mg, most preferably comprises TG2 inhibitor at a daily dose of 200 mg.

27. The computer-implemented method according to any one of the claims 1 - 26, wherein the transglutaminase 2 inhibitor is a reversible transglutaminase 2 inhibitor or an irreversible transglutaminase 2 inhibitor.

28. The computer-implemented method according to any one of the claims 1 - 27, wherein the transglutaminase 2 inhibitor is (S,E)-methyl-7-(1 -(2-(2-ethylbutylamino)-2-oxoethyl)-2-oxo-1,2-dihydro-pyridin-3-ylamino)-6-(1-methyl-1 H-imidazole-5-carboxamido)-7-oxohept-2-enoate (Compound 1):Compound 129. The computer-implemented method according to any one of the claims 1 - 28, wherein the therapy regimen comprises at least the use of a pharmaceutical composition comprising the TG2 inhibitor as an active ingredient, together with at least one pharmaceutically acceptable carrier, excipient and / or diluent in the treatment of celiac disease of said subject, preferably wherein the pharmaceutical composition is a systemic formulation.

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