KIT and gastrointestinal stromal tumor: Our findings that TKI258 can inhibit FGFR kinases incorporating gatekeeper substitutions (Fig. 1, Fig. 2, Fig. 4) suggest that it could be also considered as a second-line treatment following failure of imatinib in GIST patients because one of the frequent causes of such failure is the intrinsic resistance mutation in the related KIT target, affecting the gatekeeper residue (Tamborini et al., 2006).