It has been previously shown that in Akita mice ER stress-induced apoptosis is mediated via CHOP; however, CHOP expression was increased only after development of diabetes, but not during the neonatal period (Oyadomari et al., 2002), further suggesting that young β-cells adapt to chronic ER stress without robust stimulation of the terminal, pro-apoptotic UPR. The gene discussed is DDIT3; the disease is diabetes mellitus.