Patients with inactivating mutations of AKT2 develop hyperinsulinemia, hypodystrophy, and early onset diabetes [1], and we used metabolic profiling of AKT2 KO hPSC-ECs to show the expected decrease in glucose catabolism (higher levels of G6P and a tendency toward higher ATP levels). The gene discussed is AKT2; the disease is Hyperinsulinemia.