This deterioration allows for the influx of antigens and microorganisms, prompting increased expression of inflammatory mediators (e.g. TNF-α, IL-1β, IFN-γ, IL-10, IL-6 and IL-12) that drive the pathogenesis of DSS-induced colitis (Tlaskalová-Hogenová et al., 2005; Perše and Cerar, 2012). This evidence concerns the gene IFNG and colitis.