Based on these findings, we can postulate a possible working model (Fig. 8D) that articular chondrocytes following ischemic ON respond to hypoxic and oxidative stresses by producing HMGB1 in addition to IL‐6, and that other proinflammatory cytokines, IL‐1β and TNF‐α, are also involved in the pathogenesis of LCPD with significant correlation to IL‐6 in the synovial fluid. This evidence concerns the gene TNF and Legg-Calve-Perthes disease.