However, in the context of disease, where plasticity between phenotypes appears to be the norm, rather than the exception, double positives, such as IFNγ/IL17A often appear in pathological states such as in the context of murine colitis, where the accumulation of IL-17A+ IFNγ+ seems to occur in an IL-23 dependent manner (Ahern et al., 2010). This evidence concerns the gene IFNG and colitis.