Inflammatory insults such as pro-inflammatory cytokines contribute to T1D pathogenesis, and others have shown that treatment of mouse and human pancreatic islets and β cell lines with cytokines (IL1β, IFNγ, TNFα, IFNα) recapitulates many of the in vivo molecular changes seen in early and late stages of T1D (4, 5). The gene discussed is IFNG; the disease is type 1 diabetes mellitus.