There is an average of 40–60 somatic mutations in coding regions, most of them in ‘passenger’ genes, but a few in cancer ‘driver’ genes, involved in activating key signaling pathways for hepatocarcinogenesis such as those implicated in telomere maintenance, cell cycle control, chromatin modification, and oxidative stress, with WNT–β-catenin, transforming growth factor-β (TGF-β) signaling and receptor tyrosine kinase (RTK) signaling cascades being relevant, among others [11,12,13,14]. The gene discussed is TGFB1; the disease is cancer.