Recent studies of gene signatures for response to the PD-L1 inhibitor therapy (atezolizumab) in urothelial cancer (UC) [20,21,22], non-small cell lung cancer (NSCLC), and renal cell carcinoma (RCC) [23] revealed that the pathways most significantly associated with tumor mutation burden (TMB, a known factor correlated with response to immunotherapy checkpoint inhibitors), were cell cycle, DNA replication, and DNA damage response (DDR). The gene discussed is CD274; the disease is non-small cell lung carcinoma.