Only a small number of non‐HLA influences in MS have so far been functionally deciphered: a genetically determined increase in the levels of soluble tumor necrosis factor (TNF) receptors blocks a protective action of TNF;14 a genetic polymorphism resulting in higher IL22 binding may neutralize a protective effect of IL22;15 and tyrosine kinase 2 exomic variation decreases pro‐inflammatory signaling.16 Many genetic variants are shared across several autoimmune diseases suggesting some common pathogenesis.17 Here, IL22 is linked to autoimmune disease.