YTHDF1 and METTL3 activate the PI3K/AKT/mTOR pathway by upregulating the ribophorin II (RPN2) gene, thereby enhancing the proliferative capacity and anti-apoptotic properties of cancer cells.24 In contrast, YTHDC1 modulates this pathway by upregulating phosphatase and tensin homolog (PTEN) expression in an m6A-dependent manner, thereby inhibiting PI3K/AKT signaling.43 This evidence concerns the gene PTEN and cancer.