As an example, we demonstrated here that NDRG1 binds to both GSK-3β and Nur77 in HCC cells, resulting in reduced β-catenin degradation and subsequent nuclear accumulation; therefore approaches to inhibit these protein-protein interactions could potentially enhance β-catenin degradation and suppress β-catenin-mediated oncogenic activities with desirable anti-tumor effects. This evidence concerns the gene NR4A1 and neoplasm.