These results are reminiscent of implications of E-cadherin in collective chemotaxis in vivo,76 and that knockdown of GRHL2 or OVOL2—top activators of E-cadherin77—disrupt collective finger-like motion in vitro in lung cancer cells.29 Another potential mechanism through which E-cadherin can drive aggressive behavior is the survival of clusters in the bloodstream by ‘synoikis’, i.e., activation of survival signals through junctional adhesions between neighboring cells.78 This evidence concerns the gene CDH1 and lung cancer.