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. Here, IGF1 is linked to benign prostatic hyperplasia.