Furthermore, under high-fat diet-induced obesity in mice, the intestinal-specific deletion of MyD88 resulted in protection against the loss of IL-18 expression in the intestine (a key barrier function element), protection against the loss of expression of the antimicrobial peptide, Reg3g (an element produced by innate immunity cells to regulate host-gut microbiota interactions) and protection against the loss of Foxp3+ CD3 cells in the intestines [88]. The gene discussed is MYD88; the disease is obesity disorder.