Preclinical studies support the potential for inhibition of MCL-1 to attenuate the underlying pathogenesis of AML (48, 50, 51, 55–59), including when used in combination with BCL-2 and/or BCL2L1 (also known as BCL-XL) inhibition (60–64). The gene discussed is BCL2L1; the disease is acute myeloid leukemia.