Together, these findings support an m6A-dependent METTL3-YTHDF1-PI3K/AKT pathway regulatory axis in RCC, although direct m6A modification of individual PI3K/AKT pathway transcripts was not examined in the present study.<h4>Conclusion</h4>METTL3 drives immune evasion and promotes RCC growth by activating the PI3K/AKT pathway through an m6A-dependent mechanism involving YTHDF1. This evidence concerns the gene YTHDF1 and renal cell carcinoma.