The inducible ROS-producing Duox system works in parallel with other immune pathways, such as the Jun N-terminal kinases (JNK) pathway. JNK signaling is activated in intestinal epithelial cells of adult flies following ingestion of pathogenic Pseudomonas aeruginosa , which leads to proliferation of intestinal stem cells to compensate for apoptotic loss of mature infected cells (for a review, see Pitsouli et al., 2009 ). An interesting aspect of this pathogen in Drosophila is that, in combination with an activated oncogenic form of RAS, it can lead to overproliferation of stem cells to form tumors . Whether the elevated incidence of human cancers of the intestinal tract as a result of associated bacterial infection (Bornschein et al., 2009; Selgrad et al., 2008) is similarly influenced by RAS activation remains to be determined. Another interesting emerging theme is the elucidation of host pathways involved in detecting cell damage in the intestine, which then regulate stem cell mediated repair of the damaged epithelium. These studies have revealed important contributions of the insulin (Amcheslavsky et al., 2009 ) and TSC-TORC1 (Amcheslavsky et al., 2011) pathways, as well as of Hippo (Hpo)-mediated activation of the JAK-STAT and Epidermal growth factor receptor (EGFR) pathways (Ren et al., 2010) . Finally, experiments involving oral infection of flies with Erwinia carotovora, a natural Drosophila pathogen, suggest that gut homeostasis is maintained by active tissue repair of cell damage caused by bacteria (Buchon et al., 2009) . The observation that ROS can trigger apoptosis followed by repair in the larval gut (Gupta et al., 2010) suggests that the Duox pathway provides compensatory feedback to pathways controlling apoptosis and stem cells to ensure that host cells damaged by ROS exposure are duly replaced. Overall, these studies provide an excellent foundation for further analysis of how the gut responds to pathogens by repairing damage and differentially responding to commensal versus pathogenic bacteria.