Although, Schultheis et al. [39] reported SOCS2 activation in CML, Hansen et al. [40] have shown its redundance for generation of CML in a BCR-ABL1 driven mouse model, implying that feedback regulation by SOCS2 is deficient in this setting. This evidence concerns the gene SOCS2 and chronic myelogenous leukemia, BCR-ABL1 positive.