Approximately 3 years ago, an editorial in The Oncologist by Dr. Bruce Chabner concluded by saying that “STI571, or Gleevec, represents a monumental leap forward in cancer chemotherapy. It proves a principle. It justifies an approach. It demonstrates that highly specific, nontoxic therapy is possible. It does not guarantee success of similar efforts, because CML may not be typical of most other malignancies. And we have much to learn about maximizing its value. Congratulations to Novartis, to Brian Druker, and their colleagues for accomplishing the equivalent of the 4-minute mile. To their colleagues in the fight against cancer, are the floodgates finally open [1]?” In the past 2 months, two important events have stimulated us to revisit this concluding statement and ask whether the floodgates have opened. The first event is no less than the 50th anniversary of Roger Bannister breaking the 4-minute barrier [2]. The second is the discovery that specific mutations in the epidermal growth factor receptor (EGFR) impart sensitivity to an EGFR inhibitor, gefitinib (Iressa®)[3, 4].

The analogy of imatinib (Gleevec®) to the 4-minute mile is quite apt. For years, there was skepticism that the 4-minute barrier could be broken. Many even postulated that there was a physiological barrier that would prevent anyone from running a mile in less than 4 minutes, but a relatively obscure runner proved that it could be done. Similar to this story, in the development of Gleevec® there was enormous skepticism that inhibiting kinases would be a useful strategy [5, 6].