In this study, sophisticated computer models representing ‘virtual’ human atria, incorporating detailed electrophysiological data at the ‘ion channel’ protein level into both idealised and realistic multi-scale tissue geometries, were used to dissect mechanisms by which two mutations in the KCNJ2 gene responsible for SQTS variant 3 (SQT3) promote initiation and sustenance of arrhythmias. This evidence concerns the gene KCNJ2 and short QT syndrome type 3.