The TNBS colitis model develops with elevated Th1–Th17 response (increased IL-12 and IL-17), while DSS colitis switches from a Th1–Th17-mediated acute inflammation (increased TNF-α, IL6, and IL-17) to a central Th2-mediated inflammatory response (increment in IL-4 and IL-10 and associated reduction in TNF-α, IL6, and IL-17) [256]. This evidence concerns the gene IL6 and colitis.