Activation of AMPK reportedly inhibits mammalian target of rapamycin (mTOR), and suppression of the mTOR pathway would induce autophagy‐dependent cell death in PRLomas.10 Notably, AMPK can be activated by AMP‐mimetic 5‐aminoimidazole‐4‐ carboxamide ribonucleoside (AICAR),11 and by MET.8 The latter is a widely used treatment for type 2 diabetes mellitus.12 The function of MET is primarily associated with its activity on cellular energy metabolism. Here, MET is linked to prolactin-producing pituitary gland adenoma.