To evaluate the extent of genomic alterations that might influence β-catenin stability and activity in HCC, we interrogated two large HCC data sets, The Cancer Genome Atlas [3] and HCC cohort from Asan Medical Center [20, 21], for somatic mutations or copy number changes in CTNNB1/β-catenin itself, APC, AXIN and FGF19. The latter was included since it is part of the 11q13.3 amplicon in HCC and is thought to mediate its oncogenic effects through stabilization of β-catenin [7]. The gene discussed is FGF19; the disease is hepatocellular carcinoma.