Consistent with this, in a murine model of AML driven by monoallelic inactivation of Smc3, disease only developed once Smc3+/- HSCs were also given the proliferation-driving FLT3-internal tandem duplication (ITD) cancer mutation, although SMC3 loss alone was sufficient to cause aberrant activation of non-HSC transcriptional programs [23]. The gene discussed is FLT3; the disease is cancer.