Preclinical studies revealed that entinostat relieved the epigenetic silencing of LAT2 caused by AML1/ETO, and inhibited leukemic maintenance.679–681 Entinostat stimulated apoptosis alone and synergized with rituximab in B-cell lymphoma, with BCL2 inhibitors in HL, and with bendamustine in MM.682–684 Various clinical trials are investigating its efficacy in MDS, AML, CMML, and lymphoma. The gene discussed is RUNX1T1; the disease is lymphoma.