They demonstrated that DHA exerts a beneficial shortening and normalizing effect on QTc and APD only in LQT2 rabbits, which carry a defective IKr but have a normal functioning IKs, with no effect observed in LQT1, LQT2–5, or LQT5 – all of which have defective IKs channel function due to mutations in the α-subunit of KCNQ1 or the β-subunit of KCNE1. This evidence concerns the gene KCNQ1 and long QT syndrome 1.