Mouse knockout models demonstrate that deficiencies of either podocyte-specific genes, encoding for podocin [37], nephrin [38], and Neph1 [39] or more ubiquitously expressed genes, encoding for α-Actn4 [33], CD2AP [40] and Fyn [41] can result in podocyte dysfunction leading to progressive glomerular disease. This evidence concerns the gene ACTN4 and glomerular disorder.