Additionally, lipidomic dysregulation driven by epigenetic alterations, such as the deficiency of SETD2, a histone methyltransferase that functions as a critical tumor suppressor, accelerates sphingomyelin synthesis and accumulation, facilitating ccRCC development.11 Despite these advances, the mechanisms linking PAT-derived lipid metabolites to ccRCC progression remain poorly defined. This evidence concerns the gene PRDM9 and nonpapillary renal cell carcinoma.