AXIN1 and neoplasm: This finding may be explained by the fact that the activation of the Wnt/beta-catenin pathway in HepG2/C3A cells and PLC/PRF/5 cells is not attributed to a decrease in DKK1 expression but, rather, to mutations in the cellular components of this pathway, including beta-catenin, AXIN and APC, rendering beta-catenin degradation impossible and increasing its translocation to the nucleus and the subsequent activation of target genes involved in proliferation and tumor invasion.