One key pathogenic mechanism in antibody-mediated autoimmunity, especially in the peripheral and central nervous system, is the divalent binding, cross-linking, and endocytosis of antigen, as seen with antibodies against AChR, GlyR, NMDAR, and Iglon5 [Figure 3B (134, 208–210, 253)]. This evidence concerns the gene IGLON5 and Autoimmunity.