As in the Long-QT syndrome, genetic ablation of KCNQ1 in mice did not consistently lead to a cardiac phenotype similar to that of the observed in the long-QT syndrome in patients, which is due to differences in the functions of potassium channels between humans and mice; thus, it is not scientifically feasible to perform cardiotoxicity testing of drugs as there is a risk of inducing prolongation of the QT interval (Casimiro et al., 2001). The gene discussed is KCNA3; the disease is Prolonged QT interval.