Interestingly, we observed that myocardial virus titer was reduced in Ad-A20 treated mice on day 4, but had no significant change on day 7 or day 10 (Figure S1), suggesting the inhibition of NF-κB signaling may be beneficial to restrict virus replication at early stage of viral myocarditis, consistent with previous reports which showed that NF-κB inhibitor BAY11-7085 treatment in CVB3 infected HL-1 cardiomyocytes and HeLa cells could reduce viral progeny release [45], [46]. The gene discussed is TNFAIP3; the disease is viral myocarditis.