MyD88‐dependent signaling is known to be required for pathogen recognition and triggering subsequent inflammation, including IL‐1β production.[51, 52] Consistent with the IL‐1β blockade, Myd88−/− mice exhibited diminished IL‐1β expression in bladder tissues (Figure 6E), with almost no IL‐17A or IL‐22 production by bladder ILC3s post‐UPEC infection (Figure 6F) and uncontrolled UPEC burden during UTI (Figure 6G). This evidence concerns the gene IL17A and bacterial urinary tract infection.