Although ILC3s remain the dominant IL-22-producers in the gut at steady-state and in response to DSS,153 the identification of specific commensals and/or microbial factors that can enhance γδ LPL secretion of IL-17 and IL-22 may allow for an enhanced antimicrobial response early in disease development to limit the severity of intestinal inflammation. The gene discussed is IL22; the disease is inflammation.