This is a primary example of an invention in translational medicine, where a breakthrough in basic science is exploited and translated into a therapeutic application, in consonance with our philosophy at Ariel Fernandez Innovation. As it is well known, side effects can often be life-threatening and may well result in the termination of a drug discovery project. As it turns out, a group lead by Prof. Thomas Force found significant cardiotoxicity issues with imatinib, the "poster child" of anticancer drugs effectively used to treat chronic myeloid leukemia and other relatively rare cancers such as gastrointestinal stromal tumor (GIST). Integrating bioinformatics annotation on signaling pathways, Prof. Force tracked down imatinib's cardiotoxicity to its inhibitory activity on one of its primary targets the Abelson (ABL) kinase. In a collaborative effort with eminent scientists from U. of Texas - M. D. Anderson Cancer Center, Ariel Fernandez (then a professor at Rice University) and his colleagues managed to rationally modify the chemical scaffold of imatinib with two goals in mind: a) retaining full anticancer activity against GIST; b) removing the inhibitory activity against the ABL kinase, identified as the culprit for cardiotoxicity. This was accomplished by contrasting the dehydron patterns of the KIT kinase, the primary target for GIST, with that of the ABL kinase. Ariel Fernandez found differences in the packing (dehydron pattern) of both kinases, differences that would not be apparent in a standard structural analysis since both kinases have a common ancestry. Then, using the wrapping technology, Ariel Fernandez redesigned imatinib so that the resulting compound would retain affinity against KIT but have no significant activity against ABL. The emerging compound named WBZ_4, synthesized in the lab of Prof. William Bornmann at M. D. Anderson Cancer Center, proved to have precisely the reactivity profile predicted by Ariel Fernandez. An animal model for GIST was constructed in the lab of Profs. Gabriel Lopez-Berestein and Anil Sood (M. D. Anderson Cancer Center) and the wrapping compound proved to be a potent anticancer agent with no cardiotoxicity, in contrast with imatinib. A plethora of licensing opportunities is emerging for this compound but what is even more important is that it constitutes a formidable proof of concept that we can remove side effects through rational design and control drug specificity to unprecedented levels.