Notably, the APD in the presence of D96V-CaM and 4,9ahTTX was still prolonged relative to baseline levels, as evidenced by WT CaM dialysis, delineating the respective contributions of LTCC and NaV1.6 dysregulation to LQT and arrhythmias in calmodulinopathy. This evidence concerns the gene SCN8A and Arrhythmia.