AKT1 and lipodystrophy: However, knocking out all adipocyte AKT activity by simultaneously deleting AKT1 and AKT2 in adipocytes, elicits an even more severe lipodystrophy phenotype, showing that AKT also regulates mTOR-independent adipocyte activities and that mTORC1-AKT interplay contributes to adipose tissue maintenance [88].