Consequently, we have analyzed the effect of Gal3 in the LPS-induced model of endotoxemia (5 mg/kg) including (i) mortality rate, (ii) acute effect of LPS challenge (1 h) on membrane-bound Gal3 on circulating immune cells, (iii) delayed effect of LPS challenge (36 h) on Gal3 expression on peripheral organs, (iv) overall pro-inflammatory and anti-inflammatory status, and (v) peripheral organ integrity. The gene discussed is LGALS3; the disease is serum lipopolysaccharide activity.