Indeed, despite its abovementioned crucial role as a tumour suppressor, APC can be dispensable for the downregulation of β-catenin/Armadillo under certain conditions, most notably in colorectal cancer cells that express APC truncations (retaining partial APC function; see below): if Axin or Axin2/Conductin are overexpressed in these APC mutant cancer cells, they are capable of destabilizing β-catenin, thereby restoring low Wnt pathway activity [19,20,22]. This evidence concerns the gene AXIN1 and neoplasm.