AKT1 and gastric cancer: Based on published research, the mechanisms by which FTO is involved in gastric cancer development include: FTO promotes the demethylation of caveolin-1, CDKAL1, and mitochondrial dynamic metabolism through m6A modification or enhances gastric cancer cell proliferation, metastasis, and chemoresistance by reducing the methylation of integrin β1 (ITGB1)[26–28]; FTO also enhances PI3K/Akt signaling to promote gastric cancer cell proliferation and migration.[29] These findings suggest that FTO can serve as an effective prognostic biomarker for gastric cancer.