Throughout its history, chronic myeloid leukemia (CML) has set precedents for cancer research and therapy, ranging from the identification of the first specific chromosomal abnormality associated with cancer to the development of imatinib as a specific, targeted therapy for the disease.¹ In this issue of the Journal, two articles²,³ continue this tradition by describing how an understanding of resistance to imatinib has led to a strategy for circumventing resistance. These articles — one concerning nilotinib and the other dasatinib — are of fundamental importance for at least three reasons. First, they provide immediate hope for patients in whom CML . . .