Gal3 (galectin-3) has been known to be involved in the regulation of kidney, lung and liver fibrosis. We have reported a novel mechanism by which Gal3 contributes to fibrogenesis. Extracellular Gal3 is required for tethering of apoptotic bodies by HSC via cross-linking with integrin αvβ3, and consequently promoting HSC activation. On the other hand, phagocytosis induces Gal3 production by both HSC and Kupffer cells. Taken together, Gal3 may become a therapeutic target for antifibrogenic strategy.