These data are consistent with the previous literature, suggesting a low frequency of KRAS mutations in ICC tumors.29,30 In addition, exon sequencing data from the MSKCC cohort demonstrated that frequent known oncogenic drivers in ICC, such as IDH1, IDH2, CDKN2A, TP53, BRAF, FGFR2, and KRAS, were infrequently mutated in early-onset ICC versus late-onset ICC patients. Here, IDH2 is linked to intrahepatic cholangiocarcinoma.