To further evaluate the reciprocal effect between these two pathways and the role of NF-κB/STAT3-mediated G6PD overexpression in ccRCC growth, 786-O cells were stimulated with the STAT3 signaling activator (IL-6) or inhibitor (STATTIC) to promote or inhibit STAT3 phosphorylation, respectively. This evidence concerns the gene G6PD and nonpapillary renal cell carcinoma.