In addition to the inhibitory activity of sunitinib against constitutively active KIT exon 9 and exon 11 mutants commonly found in naive GIST cells [34], this RTKi also potently inhibited exons 13 and 14 mutant variants of KIT (i.e., V654A and T670I), which are known to be associated with reduced binding affinity and resistance to IM [35,36,37]. The gene discussed is KIT; the disease is gastrointestinal stromal tumor.