Expression of Cdh1 as well as a second component of AJs, Jup, was retained in both the non-invasive IT tumors and in the now more prevalent focally invasive IC1 tumors following genetic deletion of Dsp. It would seem likely, in light of the aforementioned functional study in this same mouse model of cancer [8], that the preservation of Cdh1 expression and of AJ function serves to maintain an additional, stronger brake on tumor invasion. Here, CDH1 is linked to neoplasm.