In addition to the genes described here in more detail, there are other promising candidates for the second causal gene in Fam2 (see Table 2). For example, of the PKP2-related genes, NOTCH2 and SCN5A harbor one of two compound heterozygous variants that have been reported to cause congenital heart disease and isolated conduction disease, respectively [51, 52]; DMD harbors a neutral hemizygous variant in the affected Fam2 individual, a gene where recessive variants can cause muscle dystrophy; DAG1 and MKKS are associated with recessive diseases, yet the variants in the affected individuals are heterozygous; IRF1 is associated with non-cardiac diseases; DSC1, a desmosomal gene not associated with heart disease, harbors a common missense variant that is predicted neutral. Since all of these genes are interesting candidates for follow up studies, it would be interesting to test whether the same or other rare variants in our candidate genes can be identified in a large cohort ACM patients, both in patients carrying desmosomal mutations or other ACM related mutations as well as in genetically unsolved cases.