The results revealed that glycolysis/gluconeogenesis and amino acid metabolism pathways were significantly upregulated in post‐ICB residual tumor cells (Figure S3D–F, Supporting Information), emphasizing the contributions of hypoxia and metabolic reprogramming in ICB resistance of RCC.[32] Clustering of stromal cells unravels the infiltration of FLT1+ ECs in ICB‐resistant tumors (Figure S4A–C, Supporting Information), which functioned as angiogenic ECs (Figure S4D, Supporting Information), and might be related with ICB resistance. The gene discussed is FLT1; the disease is renal cell carcinoma.