In this study, we show that, mirroring the widespread yet heterogenous down-regulation of the UCEs in patients with HCC, a collection of HCC mouse models displayed divergent UCE expression levels, with substantial repression in several carcinogenic and oncogenic models including those driven by β-catenin but not by silencing the tumor suppressor Axin1 (Fig. 1). The gene discussed is AXIN1; the disease is hepatocellular carcinoma.