EFNB2 and pulmonary fibrosis: Although EphrinB2 emerged as a potent pro-fibrotic factor in the both organs after injury, EphrinB2 contributed to cardiac fibrosis through a phosphorylation-dependent signaling, leading to the transition of cardiac fibroblast to myofibroblast [15], while in lung fibrosis, fibroblast-derived EphrinB2 was cleaved as a soluble type to activate EphB forward signaling in an autocrine way [29].