Although the mechanism of G6PD in ccRCC was not fully revealed, it was faithful that in addition to the proliferation-promoting effect, the work model unraveled in present study—NF-κB and pSTAT3 synergistically drove G6PD overexpression (Fig. 7)—might display more functions, especially the potential to mediate tumor metabolic reprogramming and facilitate metastasis of ccRCC patients. This evidence concerns the gene NFKB1 and nonpapillary renal cell carcinoma.