The mechanisms underlying the redistribution of β2-adrenoceptors and LTCCs away from the t-tubules, resulting in a more uniform distribution across the cell membrane, are unclear; presumably, the redistribution of Cav-3 to noncholesterol-rich membranes in heart failure leads to a loss of Cav-3 from the t-tubules and the consequent disruption of Cav-3-dependent complexes containing LTCC/adenylyl cyclase/PKA/β2-adrenoceptors (29). The gene discussed is CAV3; the disease is heart failure.