AKT1 and benign prostatic hyperplasia: The underlying mechanism is as follows: IGF‐1 activates AKT phosphorylation at multiple sites on TSC2 to inhibit the GTPase activity of TSC2, leading to the activation of mTORC1.26 In addition, PI3K activation in the IGF‐1/AKT pathway also upregulates mTORC1, thereby inhibiting the downstream autophagy signalling pathway.27 Unfortunately, whether IGF‐1 regulates BPH via the autophagy pathway remains unclear.