Because high-concentrate feeding can result in increased plasma concentrations of lipopolysaccharide binding protein (LBP) [18], a proxy for increased LPS entry to the bloodstream (i.e., endotoxemia), we speculate that the induction of the proinflammatory state that promotes SM degradation may be the result of LPS activation of toll-like receptor-4 signaling and TNFα [28]. The gene discussed is TNF; the disease is serum lipopolysaccharide activity.