In summary, our findings demonstrate that IGF2BP3 may stabilize the expression of AGAP2-AS1 through m6A modification, and up-regulate THBS2 by competitively binding to miR-9-5p, thereby activating the PI3K/AKT signaling pathway, and ultimately inducing the polarization of macrophages M2 and promoting the occurrence and development of ccRCC (Fig. 7). This evidence concerns the gene AKT1 and nonpapillary renal cell carcinoma.