More specifically, the targeted pharmacological inhibition of class I HDAC isoforms, especially of HDAC1, HDAC2, HDAC3, and HDAC8 on melanoma cell lines, prompted an upregulation of PD-L1 and PD-L2 on tumor cells by increasing the acetylation levels of their regulatory regions, leading to chromatin relaxation, and the enhancement of gene expression [23]. The gene discussed is HDAC3; the disease is neoplasm.