BCR-ABL-independent resistance might develop through upregulation of the PI3K/AKT/mTOR pathway.48 At this point, PI3K/AKT/mTOR pathway inhibitors might be a new target for TKI resistance in CML patients.49 NVP-BEZ235 is a dual inhibitor which shows efficacy against imatinib-resistance CML by arresting the cell cycle at G0/G1 and inactivating the PI3K/AKT/mTOR pathway.50 The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.