Recent studies performed in human β-cells suggested that pancreatic IL-17 contributes to the pathogenesis of T1D by two mechanisms, exacerbating β-cell apoptosis and increasing local production of chemokines by islets exposed to pro-inflammatory cytokines (e.g., IL-1β + IFN-γ and TNF-α + IFN-γ) (45). The gene discussed is IFNG; the disease is type 1 diabetes mellitus.