HBEGF and arthritic joint disease: Integrating all these findings, we propose that too much HB‐EGF signaling may inhibit differentiation and maturation of articular chondrocytes, whereas too little HB‐EGF‐EGFR signaling may reduce the number of articular chondrocytes, both of which can disrupt the integrity of articular cartilage and leads to development of arthritis‐like phenotypes.