In 1988, Molkentin et al. generated a transgenic mouse that overexpressed a constitutively active form of CnA lacking the C-terminal autoinhibitory domain in cardiomyocytes.21 Every transgenic mouse spontaneously developed severe cardiac hypertrophy, which could be prevented by the calcineurin inhibitor cyclosporin A. Calcineurin inhibition also attenuated phenylephrine (PE)- or angiotensin II (Ang II)-induced pathological cardiomyocyte hypertrophy in vitro. This evidence concerns the gene AGT and cardiac hypertrophy.