It is worth highlighting that Torin-2 maintained a prolonged suppression of mTORC1/mTORC2 with a sustained anti-proliferative effect, overcoming the limitations of rapalogs such as RAD001, as demonstrated by our findings, which resulted in re/hyper-phosphorylation of Akt and could hamper their anti-tumor action and enhance resistance to antineoplastic therapy, thus resulting in a poor outcome [40]. Here, PRDX2 is linked to neoplasm.