The present disclosure relates to methods of treating autoimmune conditions in patients who have genetic alterations in the TNFRSF6B gene, which codes for the decoy receptor 3 protein (DcR3), for example that reduce the expression, secretion, or ligand binding activity of DcR3. For example, in some embodiments, the conditions may be treated with molecules that inhibit the activity of DcR3 ligands such as LIGHT, TL1A, and FasL, such as anti-LIGHT, anti-TL1A, and anti-FasL antibodies, or inhibitors of the non-canonical NF-κB pathway.