To further study this finding, we analysed the expression of uc.158− in the liver of mice genetically engineered to harbour deletion of Axin1. These animals (Axin1fl/fl/Cre) were shown to develop microscopic foci of HCC in the absence of nuclear localisation of β-catenin.28 In line with previous findings, we did not detect any change in the expression of uc.158− in the liver of Axin1fl/fl/Cre in comparison with WT mice (figure 2C). The gene discussed is AXIN1; the disease is hepatocellular carcinoma.