The HDAC inhibitors, butyric acid and MS‐275 (entinostat), were each conjugated to trans‐retinoic acid via an ester linkage.3 Trans‐retinoic acid induces differentiation and arrests proliferation in a wide range of cancer cells.96 The 2 retinoic acid conjugates displayed potent antiproliferative activity in a hormone‐insensitive breast cancer cell line, MDA‐MB‐231 and some drug‐resistant breast cancer cell lines, MCF‐7TAMR, MCF‐7 HOX‐B7, LTLC and LTLT‐Ca.38 The gene discussed is HDAC9; the disease is breast carcinoma.