Since, under normal physiological cellular conditions, SOS1 is known to be expressed in myeloid cells and is regulated by the ABL kinase in the processes of RTK-induced actin cytoskeleton remodeling [32], these observations of SOS1/2-KO mice provided substantial indirect experimental evidence suggesting that SOS1 may be a critical mechanistic contributor to the pathogenesis of CML. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.