The critical importance of innate immune response activation during the development of obesity-associated insulin resistance has been highlighted by the phenotype of mice with targeted disruption of the NFκB pathway in myeloid lineage cells, as well as mice deficient for the chemokine receptor CCR2, which both exhibit reduced WAT inflammation and are therefore protected from obesity-induced insulin resistance [11], [37]. The gene discussed is NFKB1; the disease is obesity disorder.