Conversely, transgenic inhibition of CaMKII prevents structural remodeling and improves heart function following myocardial infarction (MI) [6] while knockout mice lacking the predominant cardiac CaMKII isoform (CaMKIIδ) are resistant to development of pressure overload-induced hypertrophy and/or heart failure [7],[8]. The gene discussed is CAMK2G; the disease is myocardial infarction.