Research has shown the importance of CDK9 in maintaining cell survival and proliferation of cells by promoting the continuous expression of MCL1 and c-Myc, the short half-life proteins, in AML cells.18,19 Furthermore, CDK9 inhibitors have been utilized for targeted tumor treatment and have demonstrated promising results in preclinical studies for AML treatment in recent years.18 However, previous research has indicated that the inhibitors for CDK9 were not highly selective. The gene discussed is MCL1; the disease is acute myeloid leukemia.