For example, mice with either nonfunctional or deleted TLR4 exhibit significant protection against high-fat diet (HFD)-induced glucose dysregulation [42, 43], insulin resistance [44, 45], and peripheral inflammation [46–48], though other studies indicate these mice are not protected against the entire range of metabolic and inflammatory effects of HFD [48, 49]. The gene discussed is TLR4; the disease is Insulin resistance.