Finally, several autoantibodies, for instance directed against actin, adenosine triphosphate synthase, angiotensin II type 1 receptor, protein tyrosine phosphatase receptor type O (PTPro), and nephrin, some of them also showing the ability to increase Palb [52], have also been recently implicated in FSGS pathogenesis [52–55]. Here, NPHS1 is linked to focal segmental glomerulosclerosis.