The inhibition of JAK2 reduces the levels of tyrosine phosphorylation of Shc and Gab2, and reduces activation of the RAS, PI3K and STAT5 pathways, thereby inducing apoptosis in CD34+ cell from patients with CML in blast crisis (65). The gene discussed is JAK2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.