Inflammatory insults such as proinflammatory cytokines contribute to T1D pathogenesis, and others have shown that treatment of mouse and human pancreatic islets and β cell lines with cytokines (interleukin-1β [IL-1]), interferon [IFN]γ, TNFα, IFNα) recapitulates many of the in vivo molecular changes seen in early and late stages of T1D (4, 5). Here, IL1B is linked to type 1 diabetes mellitus.