To test this hypothesis, we overexpressed or knocked down SF3B4 in cells and then treated with proteasome inhibitor MG132, and the results showed that MG132 treatment significantly increased KLF16 protein level regardless of transfection with oeSF3B4 or shSF3B4 (Fig. 6A, B), implying that SF3B4-regulated KLF16 does not undergo ubiquitin-mediated degradation in ccRCC cells. The gene discussed is KLF16; the disease is nonpapillary renal cell carcinoma.