NOS1AP and long QT syndrome 1: Mechanistically, NOS1AP overexpression shortens repolarization via decreased L-type calcium currents and increased rapid rectifier potassium currents (IKr) in isolated ventricular cardiomyocytes [27], providing a rationale for how NOS1AP sequence variants could modulate QT interval in humans, and specifically in LQT1, where the dependence on IKr to compensate for LQT1-related IKs reduction is enhanced [28].