Using a novel murine appendicitis model we developed [6], we had shown that AA provided significant protection against subsequent experimental colitis by curtailing T-helper 17 cell-recruitment, cell-differentiation, cell-activation, and cell-effector interleukin expression [7] by suppressing autophagy gene expression and gene-set expression [9], by suppressing endothelin-related genes and gene-sets [10], and by upregulating or downregulating genes and gene-sets specific to IFN activity [11]. This evidence concerns the gene IFNA1 and colitis.