The results showed that the C1 and C2 subgroups had frequent copy number variations (CNVs) in the region of oncogenes and tumor suppressor genes (e.g., VHL and TTN), as well as metabolic regulators (e.g., COL9A1 and COL19A1), suggesting that CNVs may play a significant role in the tumorigenesis and progression of ccRCC. The gene discussed is COL9A1; the disease is nonpapillary renal cell carcinoma.