In addition, defects in collagen IV α3, 4, and 5 (COL4A3, COL4A4, and COL4A5) genes traditionally causing the Alport syndrome complex are now recognized to also cause an FSGS phenotype associated with podocyte depletion [18–21], and ApoL1 gene variants prevalent in African–Americans are a major cause of FSGS phenotypes [22, 23]. This evidence concerns the gene APOL1 and focal segmental glomerulosclerosis.