Although the exact etiologies of IBD remain unknown, numerous studies have suggested that activation of the nuclear factor kappa B (NF-κB) pathway as well as excessive production of proinflammatory mediators such as nitric oxide (NO), myeloperoxidase (MPO), cyclooxygenase-2 (COX-2), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, etc., play pivotal roles in the pathogenesis of IBD [3]. The gene discussed is CCL2; the disease is inflammatory bowel disease.