Of particular interest in the context of diabetes is the observation that GLIS3 KD increases rat beta cell apoptosis under basal condition and sensitizes the cells to death induced by pro-inflammatory cytokines (IL-1β + IFN-γ), the viral by-product dsRNA, and the free fatty acids oleate and palmitate, while GLIS3 up-regulation protects against cytokine-induced apoptosis (present data). Here, GLIS3 is linked to diabetes mellitus.