Mechanistic studies revealed that 44 (Figure 23) directly induced hyperacetylation of histone 3, which led to the activation of caspase 3 and the degradation of the promyelocytic leukemia-retinoic acid receptor α (PML-RARα) fusion protein, which subsequently facilitated the apoptosis of APL and ATO-resistant APL cells. The gene discussed is PML; the disease is acute promyelocytic leukemia.