KIT and gastrointestinal stromal tumor: The ponatinib IC50 for GIST with KIT V654A was 100 nM, but this exceeds the clinically relevant concentration (<28 nM) for this drug,28 confirming previous evidence that ponatinib is not sufficiently active against this common resistance mutation.19 A broader group of TKIs (sunitinib, regorafenib, sorafenib, ponatinib and dovitinib) inhibited GIST cells dependent on the “gatekeeper” KIT exon 14 T670I mutation (IC50 5–200 nM).