Here, we revisit the regulatory relationship between APC and Axin, noting that all previous tests of Axin function were done under partial APC loss-of-function conditions: virtually all APC mutations found in cancers produce APC truncations whose Axin-binding sites are deleted, but which retain multiple β-catenin-binding modules [25], which could confer partial Wnt pathway activity, conducive to tumourigenesis [26]. This evidence concerns the gene APC and cancer.