These findings are significant because they highlight the dual action of long-term alcohol-activated JNK2 in altered myocyte Ca2+ homoeostasis, which may be able to explain a long-time unresolved mystery occurring in individuals with a long history of excessive alcohol consumption that have a high risk of developing cardiac arrhythmias, but can maintain a normal level of cardiac function for many years. The gene discussed is MAPK9; the disease is chronic obstructive pulmonary disease.