In identifying novel approach targeting of erbB3, we discovered that the class I histone deacetylase (HDAC) inhibitor entinostat specifically increased miR-125a, miR-125b, and miR-205, which acted in concert to inhibit erbB3, and subsequently induced apoptosis in erbB2-overexpressing breast cancer cells [19, 20]. This evidence concerns the gene HDAC9 and breast carcinoma.