In this issue of the Journal, Tester and Ackerman (5) present compelling data implicating a cardiac channelopathy as the pathogenic basis for 35% of SUDs, with 20% of mutations related to LQTS. They had previously reported from the same series that 15% of cases had mutations related to CPVT1 (6). The present study involved 49 cases of SUD. The average age at death was 14 years. Molecular screening, performed on DNA extracted from either autopsy blood or frozen tissue, examined the 5 genes traditionally associated with LQTS (KCNQ1, KCNH2, SCN5A, KCNE1, KCNE2), the gene for the Tawil-Andersen syndrome (KCNJ2) incorrectly labeled LQT7 by some investigators as discussed elsewhere (7), part of the gene ANK2 implicated in a complex disease improperly called LQT4, and the specific mutation on the gene CACNA1C responsible for the Timothy syndrome, also called LQT8 (8). The LQTS mutations were found in 10 SUD cases (20%). Most of these mutations are associated with the clinical variant LQT1, the remaining with the variants LQT2 and LQT3. Two of the 10 are functional polymorphisms known to confer arrhythmic risk to a vulnerable host.