In this trial, metformin was used in combination with sapanisertib as metformin activating AMP-dependent kinase (AMPK) causes phosphorylation and activation of the tumor suppressor gene TSC2, which exerts an inhibitory effect on mTOR43; pre-clinically, metformin-induced activation of AMPK has been shown to inhibit cell proliferation, reduce colony formation, and inhibit MAP kinase, AKT, and mTOR44, therefore use of metformin in this patient may have also contributed to the enhanced anti-tumor effect. This evidence concerns the gene AKT1 and neoplasm.