Here, we show that acquiring KrasG12D mutations or subsequent loss of p53 on a KrasG12D background in the pancreas is not sufficient to drive alterations to E-cadherin mobility, whereas acquisition of a gain-of-function mutation in p53 on the same initiating KrasG12D background mobilizes E-cadherin, consistent with the tumor dissolution and metastasis found in these mice. Here, TP53 is linked to neoplasm.