Based on our findings that single treatment with ponatinib, but not any of the first or second generation BCR::ABL1 inhibitors, could suppress FLT3 signaling, restore TKI sensitivity, and elicit marked cytotoxicity in BP-CML cells, we suggest a new drug application for ponatinib to treat FLT3+ CML patients. The gene discussed is FLT3; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.