We previously found that the overexpression of GS in mouse HCC is a biomarker of β-catenin activation in these tumours.[85], [86], [87] GS is also a specific biomarker of strong β-catenin activation in human HCC with CTNNB1 mutations (Fig. 2).[88], [89], [90], [91] We demonstrated that mouse β-catenin-activated livers are not addicted to glucose, from the observation that 18F-deoxyglucose-PET imaging is not enhanced in β-catenin-activated livers and tumours. This evidence concerns the gene CTNNB1 and neoplasm.