Elevated JAK3 expression activates JAK3/STAT3 signaling, and phosphorylated STAT3 subsequently upregulates oncogenes (e.g., MYC) as well as sialyltransferase ST6GALNAC5-which directly increases cell membrane sialylation, a known driver of immune evasion.<h4>Conclusions</h4>Our findings reveal the role of sialylation-immune-related lncRNAs in the immunosuppressive tumor microenvironment and cancer progression in ccRCC, providing a new framework for predicting patient outcomes and therapeutic responses. This evidence concerns the gene JAK3 and nonpapillary renal cell carcinoma.