These data demonstrated that v-Abl signaling short-circuits the CSF2 dependency of GMPBTs and alternatively activates STAT5 (summarized in Figure 4G), similarly to the major function of the human BCR-ABL translocation oncoprotein in chronic-phase CML LSCs (Hantschel et al., 2012; Hoelbl et al., 2010; Moriggl et al., 2005). The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.