Recently, a peptide inhibitor of IRF1’s interaction with KAT8, a histone acetyltransferase and interaction partner of IRF1, has been shown to inhibit PD-L1 expression and improve the anti-tumor immune response both in vitro and in vivo [34], suggesting that targeting IRF1 or its interactions may represent a promising strategy for cancer immunotherapy. This evidence concerns the gene CD274 and neoplasm.