This is supported by an observed 2–3 fold increase of circulating proinflammatory cytokines and chemokines like IL-6 and MCP-1 after a single oral gavage of ATI to normal mice or to mice with experimental inflammatory bowel disease25 Alternatively, the myeloid cells, after sensing the ATI, may migrate further towards the end-organ, here the liver (and adipose tissue), where they would directly promote metabolic inflammation, keeping in view the postulated nexus of inflammation mediated obesity and insulin resistance. The gene discussed is CCL2; the disease is obesity disorder.