Given the current use of TKI and immunotherapy as first-line treatments for advanced ccRCC [47], the roles of STAT2, STAT1, and their transcriptional factor complex in ccRCC drug resistance warrant further investigation and will be a potential therapeutic target, even including the upstream of STAT family, Janus kinase (JAK). The gene discussed is SOAT1; the disease is nonpapillary renal cell carcinoma.