In addition, IFNG, the only type II IFN and an important mediator in type 1 inflammation, as well as IFN-II-inducible genes have been shown to be overexpressed in the muscle of IBM, ASyS, and DM patients as compared to IMNM and control patients[6–11, 16, 17]. The gene discussed is IFNG; the disease is inclusion body myositis.