HDAC8 alone was implicated in the pathogenesis of neuroblastoma,19 but multiple HDACs are dysregulated in most other cancers.17,18 ChIP/re-ChIP assays in the presence of agents such as etinostat, which preferentially target class I HDACs other than HDAC8,17 might provide insights into the roles of HDAC1, HDAC2, and HDAC3 in regulating BMF expression in the absence of HDAC8. Here, HDAC3 is linked to cancer.