Knowing that the kinase activity was the key to treatment, pharmaceutical companies screened chemical libraries of potential kinase inhibitory compounds. After initially finding low potency inhibitors, a relationship between structure and activity suggested other compounds that were optimized to inhibit the BCR-ABL tyrosine kinase activity. The lead compound was STI571, now called Gleevec™ or imatinib (Figure \(\PageIndex{9}\)). This drug was shown to inhibit the BCR-ABL tyrosine kinase activity and to inhibit CML cell proliferation in vitro and in vivo. Gleevec™ works via targeted therapy—only the kinase activity in cancer cells was targeted and thereby killed through the drug's action. In this regard, Gleevec™ was one of the first cancer therapies to show the potential for this type of targeted action. It was dependent upon the genetic identification of the cause and protein target and is often cited as a paradigm for genetic research in cancer therapeutics.