Deficiency of lubricin (PRG4), the principal boundary lubricant in cartilage, contributes to progressive joint failure that is hallmarked by increased joint friction, superficial and upper intermediate zone apoptosis, and synovial hyperplasia, as shown in Prg4-null mice [1] and patients with camptodactyl-arthropathy-coxa vara-pericarditis (CACP) syndrome [2,3]. Here, PRG4 is linked to camptodactyly-arthropathy-coxa vara-pericarditis syndrome.