While much remains to be uncovered about how IL-36 mediates such diverse effects, we and others have demonstrated that IL-36 can influence CD4+ T cell responses, which contribute to the development of colitis.15,18 Infiltration of pathogenic CD4+ T cells to the intestinal mucosa is a characteristic of IBD, and accounts for much of the pathology associated with disease, rendering CD4+ T cells a key target in the development of novel biotherapeutics.23–25. The gene discussed is CD4; the disease is colitis.