To evaluate the relative importance of CCR2+ macrophage-independent NFκB signaling on contractile dysfunction in ACM, we treated 16-week-old Dsg2mut/mut and Dsg2mut/mut × Ccr2–/– mice with Bay 11-7082, a potent inhibitor of NFκB (6), for 8 weeks and assessed contractile function and arrhythmias before and after treatment. The gene discussed is CCR2; the disease is cardiac arrhythmia.