Heterozygous pathogenic COL4A3-A5 variants are commonly found in familial IgA glomerulonephritis, as the thinned glomerular BM could allow for the migration of IgA from glomerular capillaries to the mesangium [28], as well as in familial FSGS, likely due to the altered glomerular BM resulting in the loss of overlying podocytes and the subsequent development of secondary glomerular hyperfiltration [10]. The gene discussed is CD79A; the disease is focal segmental glomerulosclerosis.