In general, HU308 administration showed some benefit after LPS administration by reducing the number of adherent leukocytes in both V1 and V3 venules, adding some support to other studies using CB2 agonist administration which show a reduction in leukocyte chemotaxis, endothelial interaction and transmigration, and release of proinflammatory mediators in experimental models of endotoxemia [26–29]. The gene discussed is CNR2; the disease is serum lipopolysaccharide activity.