HDAC3 is the principal isoform controlling PD-L1 expression: its inhibition increases IFN-γ production and histone acetylation at the PD-L1 promoter, thereby enhancing PD-L1 transcription in tumor cells and elevating PD-L1 levels in dendritic cells within the tumor microenvironment. Here, HDAC3 is linked to neoplasm.