In this regard, using CML cells and mouse xenografts, we recently showed that the phosphorylation of SOS1 on tyrosine 1196 promotes its RAC GEF activity and contributes to BCR-ABL leukemogenesis [17], indicating that the BCR-ABL-pY1196SOS1-RAC axis is essential in promoting the full transformation and leukemogenic activity of the fusion protein. The gene discussed is SOS1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.