We performed cell migration experiments in which E-cadherin was independently targeted by gene knock down with shRNA, or by means of RHBDL2 overexpression in order to tackle the role of RHBDL2 in E-cadherin functional interference; in either case, we similarly observed a cell migration increase in association with E-cadherin downregulation, and this was confirmed in two distinct cancer cell models (Figure 3A–C). Here, RHBDL2 is linked to cancer.