Bartram et al. found that ACTN4 gene p.g195 d mutation in FSGS sporadic children and uroepithelial cells showed that the expression levels of α-actinin-4 was lower than those in healthy controls [9], while Wagrowska-Danilewicz et al. showed no change in α-actinin-4 expression in patients with minimal nephrotic patients, but lesions were observed in the glomeruli [14]. Here, ACTN4 is linked to focal segmental glomerulosclerosis.