Entinostat specifically has been shown to inhibit tumor growth and prolong survival in numerous preclinical models of breast cancer irrespective of molecular subtype.(29, 30) Many mechanisms of HDACi‐mediated antitumor effects have been demonstrated, including repression of Myc target genes, induction of apoptotic and autophagic cell death, cell cycle arrest, and accumulation of DNA damage.(29, 31, 32, 33) In contrast to these primary tumor studies, our findings demonstrate that metastatic growth in the bone is significantly elevated after some HDACi treatments, including entinostat. Here, MYC is linked to neoplasm.