Finally, our characterization of the population of stem cells present in the bone marrow of our transgenic mouse strains lacking SOS1 or SOS2 was consistent with our previous observations in non-CML contexts [35] and provided further mechanistic insight regarding the participation of SOS1 in CML pathogenesis by documenting the prevalent functional role of SOS1 in the control of cell renewal and proliferation of this population of hemopoietic progenitor cells, which are responsible for giving rise to the various blood cell lineages that are pathologically altered in CML. This evidence concerns the gene SOS1 and chronic myelogenous leukemia, BCR-ABL1 positive.