Based on this hypothesis, it is suggested that progression and flares of IBD are not only due to increased production of pro-inflammatory molecules IL-6, TNF-α, MIF (macrophage migration inhibitory factor), HMGB1 (high mobility group box 1), free radicals and lipid mediators such as prostaglandins (PGs), leukotrienes (LTs) but also as a result of decreased formation and release of anti-inflammatory molecules: IL-4, IL-10, TGF-β, and lipoxins, resolvins, protectins, maresins and nitrolipids. This evidence concerns the gene TGFB1 and inflammatory bowel disease.