The initial studies demonstrating the major effects of LQT9 mutations left significant questions as there are two distinct cellular mechanisms causing ionic current abnormalities: gain of INa-L due to sodium channel nitrosylation and inhibition of Kir2.1 and Kir2.2 channel membrane trafficking causing loss of IK1. How and by what mechanism do LQT9 Cav3 mutations cause a clinical ventricular arrhythmia? The gene discussed is CAV3; the disease is Ventricular arrhythmia.