BCL2 and diffuse large B-cell lymphoma: In preclinical models of DLBCL and MCL, panobinostat, belinostat, depsipeptide, and vorinostat were shown to evoke tumor growth arrest, differentiation, and/or apoptosis in vitro and/or in vivo, mediated by the accumulation of DNA damage upon PARP trapping (Valdez et al., 2018), G1 cell cycle arrest consequent to an increase in the expression of the cyclin-dependent kinase inhibitor p21, acetylation of histone H3 (Xue et al., 2016), or transcriptional activation of the BCL-2 family proapoptotic members BIM, BMF, and NOXA (Kalac et al., 2011; Xargay-Torrent et al., 2011).