Several histone deacetylase (HDAC) inhibitors have been shown to induce cell death of hematologic malignancies by modulating NOXA expression.33,37,38 Based on our findings that overexpression of NOXA via gene transfer improved the susceptibility of tumor cells to CAR T cells, we attempted to investigate whether HDAC inhibitors might obtain similar biological responses by pharmacologic upregulation of NOXA. The gene discussed is PMAIP1; the disease is neoplasm.