In conclusion, the development of IMN and its rarity in the general population may not be the result of rare genetic mutations in PLA2R, but rather a rare combination of three relatively common conditions: HLA-DQA1 confers susceptibility to autoimmunity, and polymorphisms in PLA2R produce a unique conformation identified by HLA class II on antigen-presenting cells and, as a target of the autoantibodies, produce IgG4 anti-PLA2R antibodies that activate the complement’s lectin pathway and cause podocyte damage and proteinuria [21]. This evidence concerns the gene PLA2R1 and Autoimmunity.