Furthermore, Met not only mitigates Dox-induced cardiotoxicity but also enhances its antitumor effects by suppressing cancer stem cell activity, downregulating the expression of the drug-resistant gene P-glycoprotein, and inducing apoptosis via inhibition of the mammalian target of rapamycin signaling pathway while activating AMPK (Singh et al., 2022). The gene discussed is MTOR; the disease is cancer.