During chronic inflammatory bowel diseases, Nhe3, Dra, and Sglt1 expression is inhibited by circulating proinflammatory cytokines.49–51 The inflammatory response to acute C. difficile infection leads to high serum levels of proinflammatory cytokines including interleukin-1β, IL-6, IL-8, IL-17A, interferon-gamma, and tumor necrosis factor-alpha.52 It is, therefore, conceivable that toxin-mediated inflammatory responses during CDI cause widespread transcriptional downregulation of Sglt1, Dra, and Nhe3 in the cecum and colon. Here, IFNG is linked to clostridium difficile infection.