While these studies convincingly demonstrate the negative effects of inflammation or pathogenic bacteria on NHE3 function, we have previously described an inverse relationship whereby loss of NHE3 activity in NHE3-/- mice lead to spontaneous, bacterially mediated distal colitis [24], greatly increased susceptibility to DSS-mediated epithelial injury [25], increased bacterial-epithelial adhesion, and changes in the mucous structure and enhanced bacterial translocation [24, 26]. Here, SLC9A3 is linked to distal colitis.