The important role of Gab2 downstream of Bcr-Abl is illustrated by the observations that its genetic depletion prevents the transformation of murine myeloid progenitors by the fusion kinase [17] and slows down the proliferation of primary human CML cells and the CML cell line K562 [9,24]. The gene discussed is GAB2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.