Thus, we hypothesize that dystrophin gene mutations that truncate the Dp427 dystrophin isoform, disrupt NaV1.5–α1-syntrophin–Kir2.1 interactions, altering the function of the most important ion channels controlling cardiac excitability and conduction velocity (CV), which would place the DMD patient at risk of arrhythmogenesis and SCD. Here, DMD is linked to Schnyder corneal dystrophy.