KIT signaling can substitute for BCR/ABL tyrosine kinase activity to activate survival signals, and governs the differential sensitivity of mature or primitive CML progenitors to tyrosine kinase inhibitors.4, 5 In this study, we showed that the PPFIA1 protein can activate several signaling pathways, including those involving KIT, Akt, and ERK1/2 in CML cells. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.