During sepsis, AGP promotes the anti-inflammatory response by binding to the adhesion molecule L-selectin, decreasing neutrophil migration and rolling, granulocyte extravasation, and recruitment of T-cells to the endothelium or of platelets to the infection site, and modulating nitro oxide-dependent pathways and glycan moiety composition [8, 11, 12]. This evidence concerns the gene SELL and Sepsis.