Interestingly, in a model of constitutively active Akt, mouse β-cells showed increased β-cell mass and proliferation via cyclin D1 and cyclin D2 with increases of p21Cip1 and p16Ink4a (66), however, another study demonstrates that mice with reduced p21Cip1 in the setting of constitutively active Akt signaling showed fasting and fed hypoglycemia, hyperinsulinemia and improved glucose tolerance (65). The gene discussed is AKT1; the disease is Hyperinsulinemia.