Therefore, patients with ACTN4 mutations develop an autosomal dominant form of FSGS, presenting with subnephrotic proteinuria, foot process effacement, and initial proteinuria or nephrotic syndrome in early adulthood, which often progresses to renal failure without ocular, neurologic, or myopathic deficits [9, 21, 22]. The gene discussed is ACTN4; the disease is focal segmental glomerulosclerosis.