In both genetic (leptin receptor deficient db/db mice) and HFD-induced type 2 diabetic murine models, Chop deletion improves β-cell ultrastructure, function, and survival, suggesting that CHOP is a fundamental factor that links ER stress to apoptosis in β cells under conditions of increased insulin demand in type 2 diabetes (Song et al. 2008). The gene discussed is DDIT3; the disease is type 2 diabetes mellitus.