In sum, our data indicate that acquired resistance to ABT-199 in AML stems directlyfrom a shift in cellular anti-apoptotic dependencies away from BCL-2 and towardMCL-1 and/or BCL-XL, as the cell struggles to maintain anti-apoptoticequipoise in the face of BCL-2 inhibition. The gene discussed is BCL2L1; the disease is acute myeloid leukemia.