Studies supporting overlapping roles for the different Akt isoforms (reviewed in [39]) include those conducted by Chen et al., who showed that haploinsufficiency of Akt1 in Akt2−/− mice causes hyperinsulinemia and hyperglycemia and that this is partly due to lipodystrophy and leptin deficiency; hyperinsulinemia and hyperglycemia were reversed in Akt2−/− and Akt2−/−;Akt1± mice when Akt1 was hyperactivated [40]. This evidence concerns the gene AKT1 and hyperinsulinemic hypoglycemia, familial, 4.