Indeed, loss of podocin, as well as inactivating mutations on its gene, are associated with glomerular lesions (including mesangial proliferation), glomerulosclerosis, albuminuria, hypercholesterolemia, hypertension, and renal failure, which characterize nephrotic syndrome [212,213,214,215,218]. This evidence concerns the gene NPHS2 and familial hypercholesterolemia.