Furthermore, BECs produce inflammatory mediators that recruit KCs to the injury area.187–189 In CCl4-induced liver injury, deletion of YAP/TAZ in BECs hinders the recruitment of phagocytic macrophages, impairing necrotic cell clearance and ultimately leading to regeneration defects at injury sites.190 Besides, BECs have been identified as the main source of osteopontin (OPN) following PHx, which activates macrophages to produce IL-6 and supports liver regeneration.191–193. Here, TBCE is linked to injury.