JOA inhibits proliferation and induces G0/G1 cell-cycle arrest and differentiation in both imatinib-sensitive and -resistant CML cells, including those with the BCR-ABL-T315I mutation, by suppressing BCR-ABL/c-MYC signaling. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.