Various researchers have been proposing other models, which are most likely not opposing the model of steric hindrance but rather complementing observed pathologies in pemphigus: the Dsg non-assembly depletion hypothesis describes how divalent anti-Dsg antibodies cross-link and cluster Dsgs, leading not only to internalization of non-junctional membrane-bound Dsgs but also resulting in prevention of incorporation of newly synthesized Dsgs into forming desmosomes (264, 265). This evidence concerns the gene DSG1 and pemphigus.