Mechanistically, RUNX1 was a transcriptional suppressor of PLCL1, LCOR could interact with RUNX1 to relieve RUNX1-mediated repression of PLCL1, leading to increased PLCL1 expression, which, in turn, inhibited the tumor progression and lipid accumulation in ccRCC. This evidence concerns the gene LCOR and nonpapillary renal cell carcinoma.