On the other hand, the QJ interval (early repolarization, which is produced by K+ efflux and once prolonged, sensitizes to ventricular arrhythmias (28)) was significantly prolonged in infected WT but not in infected Il-1r−/− mice, indicating that IL-1β signaling through IL-1R is critical to prolonging ventricle repolarization interval in Chagas disease (Figures 2A, B). The gene discussed is IL1B; the disease is Chagas disease.