A selective HDAC3i developed by the Broad Institute (BRD3308/OKI422) has demonstrated promising activity both in vitro and in vivo. HDAC3 inhibition increased H3K27Ac, transcription of B-cell-terminal-differentiation genes, MHC-II expression, and inhibited cell proliferation of lymphoma cell lines even in the absence of a CREBBP mutation, although these effects were more marked in CREBBP-mutant lines (Mondello et al., 2020). This evidence concerns the gene CREBBP and lymphoma.