This is demonstrated by the severe perturbation of intermolecular communication between EF2 and the interface with RyR2, observed for all LQTS mutants analyzed in this study, independent of the position of the mutation, and by the severely decreased EF1-RyR2 communication shown by the D129V CaM variant, for which the binding process was especially unfavorable and hardly detectable. This evidence concerns the gene EEF2 and familial long QT syndrome.