Such a mechanism is observed for desmoglein-3 in the life-threatening dermatosis pemphigus vulgaris, where the inhibition of cadherin adhesion (resulting from interaction of anti-cadherin auto-antibodies) leads to cadherin internalization and degradation, while plakoglobin steady state levels remain unaltered [16,35]. Here, CDH17 is linked to pemphigus vulgaris.