The results suggest that mutated Wisp3 protein aggregated abnormally in cytoplasm, and mutated Wisp3 failed to inhibit cell proliferation and modulate the expression of type II collagen in chondrocytes, which may be an important molecule mechanism involved in the pathogenesis of SEDT-PA/PPD. The gene discussed is CCN6; the disease is progressive pseudorheumatoid arthropathy of childhood.