The pathogenic mechanisms underlying idiopathic nephrotic syndrome (INS) in children, or minimal change disease (MCD) or primary focal and segmental glomerulosclerosis (FSGS) in children and adults, have been intensively investigated. Remarkable progress by geneticists identified multiple monogenetic variants that explain a fraction of these disorders, particularly in children.1 While the pathogenesis of noncongenital disease remains elusive, there is compelling evidence to suggest that at least 1 mechanism underlying INS, MCD, and FSGS involves immunological dysregulation and/or a circulating factor.