Immune checkpoint inhibitors (ICIs), such as PD-1, PD-L1, and CTLA-4 blockers, restore cytotoxic T cell–mediated surveillance by disrupting inhibitory signals within the tumor microenvironment (TME), and have shown promising efficacy in RB, where PD-L1 is upregulated and co-expression of PD-1/CTLA-4 correlates with poor prognosis (77, 78). The gene discussed is CTLA4; the disease is neoplasm.