On the other hand, IFN-γ, identified as a major mediator initiating colitis in IL-10−/− neonates [5, 27], showed increased levels in IL-10−/− mice as a result of failed regulatory T cells production or even functionality in the absence of IL-10, suggesting that Th1 cells are activated very early in the disease process [27]. This evidence concerns the gene IFNG and colitis.