Genetic and pharmacological inhibition of SREBF1 and SREBF2 activity also reduced ccRCC proliferation, suggesting that effects on lipid metabolism explain at least partially the phenotypic consequences of KLF6 depletion, although our results do not exclude the possibility that KLF6 promotes ccRCC growth through other mechanisms as well. The gene discussed is SREBF1; the disease is nonpapillary renal cell carcinoma.