Histone deacetylase (HDAC) inhibitors, e.g., entinostat (SNDX-275), have been recognised as cell “switches” that can reverse the therapeutic response of cancer cells from insensitive to sensitive when combined with cancer therapeutics.11 Our group studied this activity of entinostat in a preclinical trastuzumab-resistant HER2+ breast cancer model, in combination with lapatinib.12 The drug combination had anti-tumour efficacy against HER2+ cell lines that were resistant to single-agent trastuzumab or lapatinib. This evidence concerns the gene ERBB2 and neoplasm.