Several recent studies highlighted a critical role for the de novo expression of CD9 and, subsequently, of CD44 as a pathogenic switch of PECs from a quiescent to an activated phenotype in CGN and in FSGS [16,51,52], confirming the pathogenic role of PECs in these diseases and offering new molecular targets for glomerular disease therapy. Here, CD44 is linked to focal segmental glomerulosclerosis.