In 1996, Druker and colleagues¹ published the initial report on the inhibitory effects of a compound later named imatinib, a BCR-ABL inhibitor that reduced proliferation of BCR-ABL–positive chronic myeloid leukemia (CML) cells in vitro. The concluding paragraph of their report captures the compelling promise of targeted anticancer therapy: “This compound serves as an example of a drug that was rationally designed to inhibit the function of a specific protein when the protein’s function was known to be involved in the pathogenesis of a specific disease state. It is hoped that by directing therapy toward the underlying disease mechanism, this will result in more effective and less toxic therapies.”^1(p565)

1996年，Druker及其同事¹发表了有关后来被称为imatinib的化合物的抑制作用的初步报告，imatinib是一种BCR-ABL抑制剂，可抑制BCR-ABL阳性慢性髓性白血病（CML）细胞在体外的增殖。他们报告的最后一段抓住了靶向抗癌治疗的有力前景：特定的疾病状态。希望通过将治疗引向潜在的疾病机制，这将导致更有效和毒性更低的疗法。” ^{1 （p565）}