Aims: We previously found that complement components are upregulated in the myocardium of patients with arrhythmogenic right ventricular cardiomyopathy (ARVC), and inhibiting the complement receptor C5aR reduces disease severity in desmin knockout (Des-/-) mice, a model for ARVC. The gene discussed is C5AR1; the disease is Arrhythmogenic right ventricular dysplasia.