From these observations showing that NAADP and TPC2 appear to participate in the effects of the β-adrenoreceptor agonist isoproterenol to increase the amplitude of Ca2+ transients in electrically stimulated myocytes, and taking into account the finding that arrhythmias caused by isoproterenol could be suppressed by the NAADP antagonist BZ194 (34), we hypothesized that isoproterenol-mediated increases in NAADP acting via TPC2 proteins might also be involved in the susceptibility to cardiac arrhythmias in the intact heart. The gene discussed is TPCN2; the disease is chronic obstructive pulmonary disease.