One of the reasons for this phenomenon is the immunosuppressive environment at the tumor site, which can be mediated by the expression of immune checkpoint molecules, such as programmed death-ligand 1 (PD-L1, CD274) acting on its cognate receptor PD-1 (CD279) on the immune effector cells.1 PD-L1 can be present either directly on cancer cells or on other cells in the tumor microenvironment (TME),2 3 making TME a formidable opponent of CAR T-based therapies. The gene discussed is CD274; the disease is cancer.