In addition, mice with urothelial-cell-specific knockout of ATG16L1 (involved in phagophore elongation), ATG7 (involved in phagophore elongation), ATG14 (involved in phagophore initiation) or Epg5 (involved in autophagosome-lysosome fusion) have no effect on bacterial load in urine at an early stage (24 h post infection), while ATG16L1 and ATG7 (but not Atg14 and Epg5) deficient mice harbor fewer UPEC QIRs (quiescent intracellular reservoirs) in the bladder at 14 days post infection13. The gene discussed is ATG7; the disease is infection.