AKT1 and Insulin resistance: Hyperandrogenism can suppress AMPK—an upstream brake on mTORC1 through TSC1/2 and direct Raptor inhibition—while insulin resistance/hyperinsulinemia drive PI3K/AKT-dependent mTORC1 activation, jointly unleashing translational programs and attenuating FOXO-mediated restraint [4,36,46].