The regulation of Cav1.2 channel expression is obviously more complex in whole animals than in cells; rats with hyperthyroidism develop cardiac hypertrophy, and decreases in the protein abundance of the α1c and Cavβ2 subunits due to proteasomal degradation have been observed in some models of hypertrophy [34]. This evidence concerns the gene CACNB2 and hyperthyroidism.