Mechanism of action of imatinib. (A) The constitutively active BCR-ABL tyrosine kinase functions by transferring phosphate from ATP to tyrosine residues on various substrates to cause excess proliferation of myeloid cells characteristic of CML. (B) Imatinib blocks the binding of ATP to the BCR-ABL tyrosine kinase, thus inhibiting kinase activity. Illustration by A. Y. Chen.