This study indicated that HDAC1 and HDAC7 were specifically overexpressed in the CSC population of breast and ovarian cancer cells, and that concomitant targeting of HDAC1 and HDAC7 by MS-275 (Entinostat) and MGCD0103 (Mocetinostat) could effectively eliminate CSCs, as these class I-specific inhibitors could suppress HDAC7 expression by facilitating its degradation [75]. The gene discussed is HDAC1; the disease is ovarian cancer.