In addition, Peng et al. [74] found that EA improved DAEA-induced IR, mitochondrial dysfunction, and endoplasmic reticulum stress in a rat model of PCOS by inhibiting the mTOR/4E-BP1 signaling pathway, and reversed the beneficial effects of EA on PCOS-like rats by inhibiting autophagy in a reversion experiment in which rats with improved symptoms were injected with 3-MA (autophagy inhibitor). Here, MTOR is linked to polycystic ovary syndrome.