Some additionalproposed mechanisms involve the extracellular matrix through activationof integrin-associated kinases, which causes repression of E-cadherinand ultimately the nuclear localization of β-catenin that eventuallydictates the behavior of the colon cancer cell.36−38 Also, trefoilfactors have been implicated in the nuclear shuttling of β-cateninin colorectal cancer irrespective of APC-mutationstatus.39 Another study suggests the CRM1mediated pathway is an additional independent nuclear transport mechanismof β-catenin.40 The gene discussed is APC; the disease is colorectal cancer.