As recent studies showed that HDAC inhibitors act in cooperation with PI3K and mTOR inhibitors to inhibit tumor growth in MYC-driven tumors [37, 38], we tested the HDAC class I inhibitor entinostat (MS-275) at a concentration ineffective for HDAC8 (500 nM) [39] and combined it with the PI3K or mTOR inhibitor. Here, HDAC8 is linked to neoplasm.