AC6 overexpression prevents cardiac hypertrophy, fibrosis, and cardiomyopathy (Roth et al., 1999; Tang et al., 2013), while cardiac-directed expression of catalytically inactive AC6 restored the detrimental effects of sustained catecholamine infusion, through diminished myocardial cAMP production (Gao et al., 2017). Here, ADCY6 is linked to cardiac hypertrophy.