NFKB1 and neoplasm: 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.