While RHBDL2 appeared as the main effector of TNFα-induced E-cadherin cleavage, our data showed that a basal level of E-cadherin shedding was visible and maintained in cancer cells also upon RHBDL2 depletion, being presumably accountable by the activity of diverse MMPs [39,40,41]. The gene discussed is RHBDL2; the disease is cancer.