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). Here, AGAP2 is linked to nonpapillary renal cell carcinoma.