By contrast, in Akita mice, a model of ER stress–mediated diabetes, glucokinase activator administration has been shown to improve ER stress–induced apoptosis in pancreatic β-cells by suppressing the expressions of CHOP and Bcl2-associated X protein (Bax) (60); highlighting the role of ER stress in the pathogeny of MODY-2. The gene discussed is GCK; the disease is diabetes mellitus.