Biochemically, active IBD is associated with upregulation of several pro-inflammatory mediators locally in the affected tissue, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6, and in more severe cases, systemic levels of these mediators have been found to be significantly elevated including C-Reactive Protein (CRP) [10,11,12]. This evidence concerns the gene TNF and inflammatory bowel disease.