However, what is known from several species is that LQTS‐associated CaM variants have been shown in several studies to increase Ca2+ influx by suppressing Ca2+‐CaM‐dependent inactivation of the L‐type Ca2+ channels, which would lead to increased SK current (Limpitikul 2014; Yin 2014; Pipilas 2016). The gene discussed is KCNN1; the disease is familial long QT syndrome.