The hypothesized mechanism for COVID-associated AAV-GN involves COVID-triggered immune dysregulation; specifically, it is possible that SARS-CoV-2 proteins promote the development of autoantibodies against neutrophil proteins such as myeloperoxidase (MPO) and proteinase 3 (PR3), which is characteristic of classic AAV-GN (178, 180–182). This evidence concerns the gene PRTN3 and ganglioneuroma.