This array of alternative inactive states provides opportunities for the development of selective kinase inhibitors, as exemplified by the success of imatinib (Gleevec, Glivec; Novartis) in blocking the activity of BCR–Abl [3] and its efficacy in the treatment of chronic myelogenous leukemia. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.