Importantly, the mutational state of these kinases can drive the choice towards the most proper inhibitor: the commonly occurring imatinib-resistant PDGFRα D842V and c-Kit D816V mutants in GISTs and mastocytosis, respectively, are more strongly inhibited in vitro by dasatinib rather than imatinib (IC50 62 vs 642 nM and 37 nM vs 3.8 μM, respectively—see Table 1 for these and other mutations), even though clinical benefits of dasatinib had been demonstrated only for the former [66]. This evidence concerns the gene PDGFRA and mastocytosis.