A variety of editing strategies have been explored to enhance compatibility with host immunity: (1) modulating HLA class I expression via B2M or HLA-E to avoid T-cell- and NK-cell-mediated clearance, (2) overexpressing CD47 to suppress macrophage-mediated elimination, and (3) disrupting inhibitory checkpoint pathways such as PD-L1, TIGIT, or CISH to improve cytotoxicity and tumor infiltration [5]. This evidence concerns the gene CD274 and neoplasm.