Second, our functional comparisons of a patient-derived ccRCC with a normal epithelial kidney cell culture as well as two VHL-defective ccRCC cell lines (786-O and RCC4) with VHL-intact derivative cell lines (786-O-VHL and RCC4-VHL, respectively) identified enhanced uptake of LDL and HDL and subsequent impairment of degradation and resecretion as the likely mechanism leading to intracellular lipid accumulation in ccRCC. This evidence concerns the gene VHL and nonpapillary renal cell carcinoma.