Imatinib was rationally designed to inhibit the PDGF receptor and the BCR-ABL tyrosine kinase (the hallmark of CML), and it was also found to potently inhibit autophosphorylation of the tyrosine kinase receptor c-KIT (involved in the pathogenesis of GIST) (Demetri et al, 2002). This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.