Overexpression of the constitutively active form of Akt1 (CA‐Akt) in β‐cells in vivo induced a significant increase in β‐cell size and total islet mass, with resultant improved glucose tolerance, which protected mice against streptozotocin (STZ)‐induced diabetes (multiple low doses of 40 mg/kg body weight for five consecutive days, which causes autoimmune diabetes).20 The gene discussed is AKT1; the disease is diabetes mellitus.