The antineoplastic effects of SAHA have been observed in various malignancies.9, 10, 11, 12, 13, 14, 15, 17, 22, 23, 24, 25, 26, 27, 28 In advanced leukemia and myelodysplastic syndrome, SAHA exposure induced significantly lower antileukemia activity than the maximum tolerated dose and inhibited the HDAC activity of peripheral blood and bone marrow blasts.29 Foster et al30 found that co‐administration of Bcl‐2 inhibitor ABT‐737 and SAHA induced apoptosis accompanied by Noxa upregulation, Bax activation, and mitochondrial dysfunction in PTEN‐intact glioma cells. The gene discussed is BAX; the disease is glioma.