KIT and gastrointestinal stromal tumor: In patients with the most common class of primary driver mutation in GIST (KIT exon 11 mutation), imatinib-resistant secondary mutations in the KIT ATP-binding pocket correlated with clinical benefit from sunitinib versus ripretinib (median PFS, 15.0 versus 4.0 months, respectively; P = 0.0005), whereas secondary mutations in the KIT activation loop indicated clinical benefit from ripretinib but not sunitinib (median PFS, 14.2 versus 1.5 months, respectively; P < 0.0001).