As AMPK inhibition using compound C was shown to reduce the phosphorylation of tuberous sclerosis complex 2 (TSC2) in cardiac hypertrophy cells and cancer cells, leading to phosphorylation of S6K1 in vitro45, and as activation of mTOR (through S6K1 phosphorylation) is well known to activate primordial follicles, it was hypothesized that inhibition of AMPK could activate primordial follicles through the mTOR pathway25. The gene discussed is PRKAA1; the disease is cardiac hypertrophy.