Importantly, E‐cadherin‐based AJs are significantly more stable than those established by N‐cadherin.[56] N‐cadherin is typically expressed by cells with mesenchymal phenotype such as fibroblasts and overexpressed in several types of cancer where it drives detachment from the primary tumor, invasion, and metastatization.[57] This similarity suggests that AJs established by PM‐YFP MDCK fail to provide sufficient mechanical stability, as normally ensured by E‐cadherin, thus delaying the jamming transition. Here, CDH1 is linked to neoplasm.