Among well‐established animal models of podocyte injury, mice that express an actinin‐4 K256E transgene in podocytes recapitulate human hereditary FSGS (Cybulsky & Kennedy, 2011), while adriamycin nephrosis is a prototypical experimental model of acquired human FSGS (Pippin et al., 2009). The gene discussed is ACTN4; the disease is focal segmental glomerulosclerosis.