Recent work has revealed that cardiac hypertrophy and failure are accompanied by decreased Cav-3 expression and loss of Cav-3-dependent stimulation of ICa (11, 21, 23), and myocytes from failing hearts commonly display impaired SR Ca2+ release (8) as a result of altered regulation of LTCCs (11), decreased t-tubular ICa density (8, 9, 11), disruption of t-tubule organization (29, 45, 47), and reduced SR Ca2+ content (3, 24, 35). This evidence concerns the gene CAV3 and cardiac hypertrophy.