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. This evidence concerns the gene BAX and maturity-onset diabetes of the young type 2.