By contrast, in tumors with mutated CTNNB1, 31 ± 27% of all ACE2 was detected at the biliary poles (Fig. 2f) and the mean dual (ACE2 + ABCC2)/DAPI signal was 35 folds higher in HCCs carrying mutated than in tumors carrying wild-type CTNNB1 (mean ± SD: wild-type, 0.0018 ± 0.004; mutated, 0.063 ± 0.07; p = 0.002), thus confirming that HCCs carrying mutated CTNNB1 are enriched in ACE2 expression and indicating that ACE2 is particularly associated with the biliary pole in tumor cells preserving polarized hepatocyte-like features. This evidence concerns the gene CTNNB1 and neoplasm.