For instance, MyD88 signaling, innate lymphoid cells (ILCs), leptin, IL-1β, IL-22, IL-25, IL-27, and IL-33, could provide protection against CDI.9–16 On the other hand, IL-17 and IL-23 could worsen C. difficile-associated severity and mortality.17,18 Together, these studies support the complexity of immune response during CDI and also suggest the potential of immunotherapeutic intervention to combat CDI. This evidence concerns the gene LEP and clostridium difficile infection.