Because no SADS case with H1153Y-KCNH2 mutation has been reported previously, and since functional study targeting this mutation has never been performed in heart disease conditions, the present paper may critically shed light on the clinical relevancy of the H1153Y-KCNH2 mutation and on its potential implications for treatment, surveillance, and follow-up in patients with hereditary cardiac channelopathies. This evidence concerns the gene KCNH2 and heart disorder.