To examine the potential for dual BCL-2 and MCL1 targeted therapy to suppress patient-derived AML in vivo, primary AML samples were xenografted into immunodeficient NOD.Rag1−/−;γcnull (NRG)-SG3 mice, which have been transgenically modified to express human SCF, GM-CSF, and IL3 in vivo, to enhance engraftment of human AML blasts [25, 26]. The gene discussed is CSF2; the disease is acute myeloid leukemia.