G6PD and nonpapillary renal cell carcinoma: The aforementioned results showed that NF-κB and pSTAT3 signaling pathways were likely to drive G6PD overexpression through the constitutively activated effect of p65 and pSTAT3, indicating that G6PD, as an important common mediator of NF-κB and pSTAT3 signaling, might become a potential therapeutic target for ccRCC treatment.