For instance, genetic autopsies have revealed gain-of-function mutations in sodium channels (Nav1.5) and type 2 ryanodine receptors (RyR2) as well as loss of function in potassium channels (Kv7.1, hERG), which are common to both sudden unexplained death in epilepsy (SUDEP) and cardiac arrhythmias [4,14,21–23]. This evidence concerns the gene KCNQ1 and chronic obstructive pulmonary disease.