Finally, this study also raises the question as to whether (regardless of the distinct gain-of-function mutation causing SQT3S), hypocholesterolemia would contribute to trigger SQT3 arrhythmic episodes by further increasing Kir2.1 availability, or if, vice versa, borderline hypercholesterolemia would reduce the severity of symptoms. This evidence concerns the gene KCNJ2 and familial hypercholesterolemia.