BRD2 and familial long QT syndrome: This general ability of N-AT to, at least partly, compensate for the reduced function of mutants with mutations in different parts of the KV7.1+KCNE1 channel complex and with seemingly different molecular defects, as long as a population of these mutant channels reaches the plasma membrane, suggests that N-AT is an interesting model compound for development of future anti-arrhythmics to treat LQTS caused by diverse KV7.1+KCNE1 mutations.