Functional analysis of the S140G-mutant KCNQ1 unveiled a gain-of-function impact on the currents of KCNQ1/KCNE1 and KCNQ1/KCNE2 channels, which significantly shorten the action potential duration of atrial myocytes thereby increasing the vulnerability to AF (Chen et al., 2003). The gene discussed is KCNQ1; the disease is atrial fibrillation.