As the selectivity of malignant cells to this combination therapy is not well elucidated, we used a cellular model of a common leukemia-associated mutation in the epigenetic regulator ASXL1 to determine the expression levels of BCL2 and investigate the mechanistic basis of BCL2 overexpression to determine whether this regulates increased sensitivity to VEN and AZA. The gene discussed is ASXL1; the disease is leukemia.