The pivotal role of Gab2 in BCR-ABL signaling is further demonstrated by observations that short hairpin (sh) RNA-mediated silencing of endogenous Gab2 inhibits the proliferation and colony formation of CD34+ cells from patients with CML, but not in cells isolated from healthy donors (59). The gene discussed is CD34; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.