Decourtye-Espiard and colleagues investigated the potential of histone deacetylase (HDAC) inhibitors as a treatment for cancers with CDH1 mutations, testing the effects of several HDAC inhibitors on gastric and breast preclinical models with and without CDH1 mutations [152], and observed greater sensitivity of CDH1-null cells than wild-type cells to pan-HDAC inhibitors, such as entinostat, pracinostat, mocetinostat, and vorinostat. Here, HDAC9 is linked to cancer.