Editors’ Note: The editors regret that in the recently published feature of Controversies in Experimental Dermatology on the question ‘‘Are desmoglein autoantibodies essential for the immunopathogenesis of pemphigus vulgaris, or just ‘witnesses of disease'?’’ (Amagai et al., Exp Dermatol 15:815–831, 2006) one commentary by H. Kurzen somehow got lost between manuscript acceptance and journal production. We apologize for this oversight, and show this commentary here in full. Also, the author list for this paper should appear in the following manner: M. Amagai, A. R. Ahmed, Y. Kitajima, J. C. Bystryn, Y. Milner, R. Gniadecki, M. Hertl, C. Pincelli, H. Kurzen, M. Fridkis-Hareli, Y. Aoyama, M. Frušić-Zlotkin, E. Müller, M. David, D. Mimouni, D. Vind-Kezunovic, B. Michel, M. Mahoney and S. Grando Once I was a strong guardian, forming solid unbreakable chains and impenetrable fences with my friends against all sorts of foes from outside to protect my dear body from all evil and danger. Then there came along a terrible enemy called pemphigus IgG that made our lines of defense give in and made us lose our arms and become vulnerable. We could not hold together anymore. First, we did not understand the nature of our enemy. Was it one? Were there many different ones? What kind of strange weapons did they use? Was there a traitor coming from within our body? The establishment said that there was only a single culprit by the name of desmoglein (1, 2), and he was, alas, coming from within. But when we took the traitor to court, he said: ‘My lord, how could I possibly have cut the arms of our line of defense? It is true, I attach to them when I come close, but I do not cause any harm.’ Is he speaking the truth? Could there be other suspects? After thorough and clandestine investigation, the revolutionaries found a whole group of offenders named phospholipase C, tyrosine kinases, calpains, caspases and acetylcholine receptors that were aiming at parts of our body that regulate our daily life. The little messenger named calcium was said to have been abused to incapacitate the arms of our impenetrable fences and even our termination machineries apoptosis and oncosis (3-6). I was shocked to hear that the enemy brings death to me and my neighbours even before we lose our arms! Should we have already begun to die before our lines of defense have broken (7)? I realized that our enemy caused changes in more than 200 functions of my body (8). Could a single offender be so powerful? Did he have any collaborators? We were sure that α9 acetylcholine receptors and pemphaxin just like the wicked Ca2+ channel blockers or ACE inhibitors were at least intimidating the little messenger (9-12). What saved desmoglein for the moment was a tale we heard from distant murine relatives that have lost their desmoglein. Our enemy still can break their lines of defense and attach to their arms. So even without desmoglein, the enemy is still mighty (13). However, we have witnesses that have seen desmoglein taking ‘phosphor’ to his serine and desmoglein himself leaving his anchor place (desmosome) after contact with the enemy (14). What made him do this? Was it desmoglein after all or one of the other offenders hiding inside the enemy? Only time will tell and, of course, our mission control centre (International Pemphigus Foundation), where the establishment and the revolutionaries exchange their hottest news and gather wisdom. This should be a tale of reason: it is not a question of winning, but of saving life! (15, 16).