In this regard, direct experimental evidence that SOS1 is critically required for CML development is now provided in this report by our in vivo observations, documenting that the genetic ablation of SOS1 (and SOS2, to a lesser extent) results in significant protection from CML development driven by p210BCR/ABL in p210 transgenic mice (Figure 2, Figure 3 and Figure 4). The gene discussed is SOS1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.