Class I HDAC inhibitors (entinostat, mocetinostat, panobinostat and belinostat) have been shown to generate robust and durable upregulation of PD-L1 and PD-L2 in tumor cells; however, this upregulation was not observed upon inhibiting Class IIa HDACs or HDAC 6 with rocilinostat, nexturastat A or PCI34051 (Woods et al., 2015). Here, HDAC9 is linked to neoplasm.