Using a primary culture of progenitor cells and normal hematopoietic counterparts isolated from the bone marrow of newly diagnosed CML patients in chronic phase and CML-blast phase cell lines, IPA-3-mediated targeting of PAK1 and/or PAK2 enhanced the antiproliferative and pro-apoptotic effect of imatinib, without affecting normal counterparts [190]. The gene discussed is PAK2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.