,13 Several studies have made the point that the failure of CPIs blocking programmed cell death 1 (PD1) and cytotoxic T-lymphocyte associated protein 4 (CTLA4) pathways in metastatic UM may be due to the higher importance of additional inhibitory pathways; while prevalence of expression of PD-L1 (the ligand for PD1) is lower in UM than in cutaneous melanoma,14 studies of primary and metastatic UM tumors have found elevated expression of TIGIT, IDO1, TIM3, and LAG3.15 The gene discussed is CTLA4; the disease is cutaneous melanoma.