The major, novel result of our study is the concomitant increase in β2-subunit expression and L-VDCC activity in three independent models: human dilated cardiomyopathy, old tg CaV1.2 mice spontaneously progressing into heart failure and young (“Adaptive State”) tg CaV1.2 mice with additional tissue-specific inducible overexpression of β2-subunits. The gene discussed is CACNA1C; the disease is heart failure.