Furthermore, myeloid progenitors from Gab2−/− mice are resistant to transformation by Bcr-Abl, indicating that Gab2 is required to sustain the leukemogenesis evoked by this oncogenic fusion protein in a model of chronic myelogenous leukemia (CML) [68]. The gene discussed is GAB2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.