The interaction between PD-L1 on tumor cells and PD-1 on T cells impedes activation, proliferation, and effector functions of antigen-specific CD8 + T cells, thus promoting cancer immune evasion.6 To systematically explore the functional residues modulating PD-L1, the core factor involved in immunotherapy, we leveraged ABEmax to generate site-directed mutagenesis for achieving large-scale screens. This evidence concerns the gene CD8A and cancer.