Results of other recent studies have called into question the idea that IL‐22 has a solely pathogenic role in arthritis, as antigen (methylated bovine serum albumin [BSA])–induced, IL‐17–mediated joint inflammation was found to occur independent of IL‐22 (43) and systemic administration of rIL‐22 was protective in late stages of disease in the CIA model (44). The gene discussed is IL17A; the disease is inflammatory response.