Recent studies by Mohler and colleagues identified rare variants in ankyrin B in patients harboring desmosomal disease, ARVC, as well as a molecular link to the cardiac cell-cell junction via beta-catenin as targeted inhibition of the Wnt/beta-catenin pathways (SB-216763) could prevent and partially rescue ARVC phenotypes in cardiac-specific ankyrin B (Ank2)-deficient mice, revealing arrhythmogenic pathways in mice distinct from classic desmosomal structural alterations and remodeling (Roberts et al. 2019). The gene discussed is ANK2; the disease is arrhythmogenic right ventricular cardiomyopathy.