Nevertheless, the inhibition of tumor growth was associated with decreased levels of G6PD, pSTAT3, and p65 in isolated tumor samples (Fig. 6f, g), demonstrating that abnormally activated pSTAT3 and NF-κB signaling pathways were positively correlated to G6PD overexpression in vivo and G6PD inhibition exhibited tumor-suppressive activities in ccRCC. Here, G6PD is linked to nonpapillary renal cell carcinoma.