Further studies showed that GC cells with high METTL3 expression are more sensitive to the mTOR inhibitor everolimus, which could reverse METTL3-induced tumor proliferation in a dose-dependent manner.[102] Feng et al. found that m6A modification and its eraser FTO may play a role in omeprazole-mediated improvement of chemosensitivity.[120] Omeprazole-induced FTO inhibition enhances the activation of the mTORC1 signaling pathway and suppresses survival-friendly autophagy, thereby improving the antitumor effects of chemotherapeutic agents on GC cells.[120]. The gene discussed is METTL3; the disease is neoplasm.