We previously demonstrated in experimental OA generated by destabilisation of the medial meniscus (DMM) that PAR2-deficient mice (PAR2−/−) were significantly protected from cartilage damage and osteosclerosis,4 subsequently confirmed by others.5, 6 While these studies showed reduced subchondral bone sclerosis in PAR2−/− mice, its role in the early stages of disease, particularly osteophyte development, has not been comprehensively investigated. The gene discussed is F2RL1; the disease is osteosclerosis.