More specifically, response to checkpoint inhibitors may be dependent on T-cell infiltration of the tumor and T-cell function in the tumor microenvironment [8], [9], as improved outcomes have been observed in patients with programmed death-(ligand) 1 (PD-[L]1)-positive tumors [10]; however, as demonstrated in anti–PD-(L)1 clinical trials [6], [11], [12], [13], many patients with advanced urothelial carcinoma do not have PD-(L)1–positive tumors. This evidence concerns the gene CD274 and neoplasm.