Class I HDAC inhibitors including panobinostat, entinostat, and mocetinostat enhanced immune therapy by durable induction of PD-L1 expression in various BRAF-mutant (WM983A, WM793) and BRAF-wildtype melanoma cells (B16F10) based on upregulated histone acetylation in the PD-L1 gene which led to chromatin relaxation. This evidence concerns the gene HDAC9 and melanoma.