PD-L1 expression can be driven by tumor-intrinsic mechanisms or induced by inflammatory cytokines, such as IFNγ, which is secreted by immune cells within the TME.3 To probe functional residues affecting cell surface PD-L1 expression in both constitutive and induced contexts, we performed screens using the S/T/Y sgRNAiBAR library in a human melanoma cell line, A375, which was engineered to stably express ABEmax. Here, CD274 is linked to neoplasm.