During the past decades, the pathogenic role of parietal epithelial cells (PECs) in focal segmental glomerulosclerosis (FSGS) and crescentic glomerulonephritis (GN) has become evident.1-3 The development of the extracapillary lesions in FSGS and crescentic GN is closely associated with PEC activation. PEC activation describes the phenotypic switch from their normal quiescent state to one in which they proliferate and migrate to the glomerular tuft, leading to glomerular injury. Typically, activated PECs are enlarged and express the glycoprotein CD44 de novo.