Because triacsin C is a competitive inhibitor of ACSLs, the reduction of exogenous lipid substrate through culturing cells with CSFBS leads to full inhibition at lower levels of triacsin C. Additionally, the increased sensitivity of ccRCC cells to triacsin C when cultured in lipid depleted media could be due to inhibition of multiple ACSL enzymes, which are active in ccRCC even if they are not required for lipid droplet accumulation, or due to inhibiting lipid droplet independent functions of ACSL3 and the ACSL family. This evidence concerns the gene ACSL3 and nonpapillary renal cell carcinoma.