Recent results have indicated that JAK2, a downstream target of BCR-Abl, can maintain activated Lyn kinase in CML via the SHP-1 pathway, suggesting that JAK2 can mediate the BCR-Abl-induced activation of Lyn and SHP-1 kinase [11]. The gene discussed is JAK2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.