Moreover, it has been shown that IM treatment activated the PI3K/ Akt/ mammalian target of rapamycin (mTor) anti-apoptotic pathway in chronic phase CML patients as well as in BCR-ABL+ Lama cells [52] and proposed that the IM-induced compensatory PI3K-Akt/mTor activation may represent a novel mechanism for the persistence of BCR/ABL-positive cells in IM treated CML patients [52]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.