Although IFNγ is increased in our model of CVB3 myocarditis in males [16, 18], we showed that elevated IFN levels in male BALB/c mice with myocarditis are mediated by IL-18, which is downstream from TLR4, rather than traditional STAT4/IL-12 transcriptional activity [18, 64]. The gene discussed is IL18; the disease is myocarditis.