Downstream signaling mediators of inflammation, such as NF-κB, are also integral to the ARVC inflammatory response as immunomodulatory therapies targeted at inhibiting NF-κB signaling show functional improvements in a DSG2 mutant-based mouse model harboring ARVC disease features (Chelko et al. 2019) (Fig. 3). This evidence concerns the gene NFKB1 and arrhythmogenic right ventricular cardiomyopathy.