It is a causative gene of familial FSGS, and mutations or loss of ACTN4 promote podocyte detachment.41, 42, 43 Here, LDHA inhibition significantly suppressed ACTN4 expression, suggesting that podocyte detachment occurs in corticosteroid-resistant FSGS via reduced ACTN4 expression and decreased energy compensation due to reduced LDHA activity. Here, ACTN4 is linked to focal segmental glomerulosclerosis.