Mutations in the AC gene (ASAH1) or deficiency of lysosomal AC activity in human cells were found to be a major genetic or pathogenic mechanism for the development of Farber disease and partially for juvenile idiopathic arthritis that were shown to develop membranous nephropathy, focal segmental glomerulosclerosis (FSGS), and minimal change disease (MCD) [35–37]. Here, ASAH1 is linked to membranous glomerulonephritis.