TERT and hepatocellular carcinoma: The key points from the above studies are: (1) TERTp and CTNNB1 mutations are concordant in patient HCC; (2) in animal models, overexpression of TERT or CTNNB1 promotes HCC, although the effect is modest in most models and often requires another oncogene or insult; (3) in cultured stem cells, TERT and CTNNB1 cooperate via direct or indirect interactions during the transcription of target genes; and (4) both CTNNB1 and, to a lesser extent, TERT, have key roles in cellular homeostasis, making the potent inhibition of endogenous genes unrealistic from a therapeutic perspective.