Therefore, their physiological roles are diverse and thus could contribute to the individual SIDS risk in more ways than just via brain edema: Loss-of-function variants in ABCC8 or TRPM4 can cause lethal cardiovascular and metabolic genetic disorders, such as congenital hyperinsulinism, Brugada syndrome, or long QT syndrome (LQTS), potentially leading to sudden infant death instead of genuine SIDS [34–39]. This evidence concerns the gene ABCC8 and familial long QT syndrome.