Supporting this latter idea, we observed that in mammals, the inverse relationship between Cas expression and total levels of E-cadherin was more notable following transient manipulations of Cas proteins (Figure 1), rather than in the context of the sustained loss of Nedd9 in mammary tumor development (Figure 7), although the failure of E-cadherin to associate with cell junctions and the detergent insoluble (membrane- and cytoskeleton-enriched) cell fraction was observed in all cases. Here, CTNND1 is linked to breast cancer.