While the exon 2 deletion in KCNQ1 (Fig 1) showed complete segregation with the LQTS, it is unlikely that the CDKL5 variant was causative of the observed epilepsy, as mutations related to this gene typically occur de novo and are associated with early-onset, severe, drug-refractory epileptic encephalopathy [10]. Here, CDKL5 is linked to familial long QT syndrome.