Quantification of mRNA expression of Cav3.1 and Cav3.2 revealed that levels up to day 5 after birth were comparable to those at the prenatal stage but had decreased by 21 days after birth and in adults.[25] In the healthy adult ventricle, the ICa,T is almost absent in working myocardium of ventricles and atria and its expression is limited to cells of the conduction system, although expression levels can be elevated under pathological conditions, such as heart failure or hypertrophy.[27]. The gene discussed is CACNA1G; the disease is cardiac hypertrophy.