Preliminary evidence also suggests that DNER overexpression may be associated with enhanced sensitivity of ccRCC cells to the PARP inhibitor Olaparib, although the underlying mechanism requires further investigation.<h4>Discussion</h4>In conclusion, DNER drives ccRCC progression by coupling glycolytic reprogramming with immunosuppressive microenvironment formation via the JAK2/STAT3 signaling axis, and may represent a potential therapeutic target for ccRCC. The gene discussed is STAT3; the disease is nonpapillary renal cell carcinoma.