At odds with this vision, however, imatinib mesylate, the first TKI to be introduced into routine praxis, initially for the treatment of CML (if positive for the ABL activating translocation or activating mutations of KIT)4 and later for that of GIST expressing activated KIT5, turned out to mediate (some of) its effects via the stimulation of NK and T cell-mediated anticancer immune responses8. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.