Evidence for involvement of TRDN in LQTS was based mainly on a single publication demonstrating 5 cases with homozygous or compound heterozygous frameshift variants.41 All cases presented during early childhood (up to the age of 3 years) with QT prolongation, negative T waves in precordial leads (Figure 2), and exercise-induced arrhythmias, although typical torsades de pointes was demonstrated only in 1 case. The gene discussed is TRDN; the disease is torsades de pointes.