Although there is no direct evidence that LPS can induce obesity via the activation of a CD14-dependent pathway, indirect observations strongly support this assumption: (i) in humans, triglyceride-rich lipoproteins contain LPS that in normal conditions is probably efficiently sequestered by soluble CD14; (ii) LPS serum levels largely increase in high-fat diet; and (iii) increased LPS levels are sufficient per se to predispose to obesity, insulin resistance, and type-2 diabetes (Cani et al., 2007). The gene discussed is CD14; the disease is Insulin resistance.