In this study, to better understand how to interpret secondary findings of variants in KCNQ1, we utilized currently published large cohorts of LQTS patients with reported genetic variants in KCNQ1, and the large gnomAD public database representing an unselected population with KCNQ1 genetic variants to determine whether missense variants within specific topological regions of the KCNQ1 encoded Kv1.7 potassium channel may provide predictive power for the likelihood of disease. This evidence concerns the gene KCNA3 and familial long QT syndrome.