The antikinase drug imatinib specifically binds to the inactive conformation of the Abelson tyrosine kinase and does not only inhibit the catalytic activity of the Bcr-Abl fusion protein but also that of other closely related Src kinases.3 By contrast, T cells recognizing the fusion peptide have the potential of being truly cancer-specific. However, as described by Popvic et al, sufficient amounts of the appropriate peptide must be generated by the proteasome, and the peptide must bind to the patient's MHC with high affinity, so that T cells can eradicate clinically relevant cancer in vivo.1
