Additionally, increased paracellular flux through the leak pathway is upregulated in response to T cell-mediated increases in TNFα and IFNγ.33,53 These findings lead us to hypothesize that host inflammatory responses during CDI may increase paracellular efflux through the leak pathway, and decrease solute absorption by NHE3, DRA, and SGLT1 in the colon, leading to coordinated dysfunction and malabsorptive diarrhea. The gene discussed is SLC26A3; the disease is clostridium difficile infection.