Parts of beneficial effects of vitamin D on cardiac pathologies, including hypertrophy, ischemia, arrhythmias, and heart failure, have been attributed to a relief of ER stress and related inflammation and cell apoptosis through VDR activation and downregulation of downstream targets, caspase, and CHOP gene expressions [35,36,37,38,39]. This evidence concerns the gene DDIT3 and Arrhythmia.