Furthermore, a recent study using the same cMyBP-C-/- mouse model as used in our study, suggests that remodeled K+ currents in adult cMyBP-C-/- hearts are the result of altered expression of K+ channels and contribute to the incidence of SCD in HCM (Toib et al., 2017). The gene discussed is MYBPC3; the disease is Schnyder corneal dystrophy.