KCNQ1 and sudden infant death syndrome: Similarly, recent evidence reported that Cnx43 together with KCNQ1 is part of the same signalling pathway that provides cell protection after myocardial infarction by acting in a functionally dependent manner.3, 29, 36 Indeed, mutations in both genes encoding for KCNQ1 and Cnx43 have been associated with clinical sudden infant death syndrome (SIDS), for which hypoxia is a major risk factor.37, 38 The data presented, therefore, identified telmisartan as a regulatory candidate of these two important factors in the infarcted myocardium, Cnx43 and KCNQ1.