The balance between the two angiotensin converting enzymes has been highlighted by ACE2 deletion murine models, which have a significantly higher mortality rate post-MI than wild-type mice. Mortality was associated with enhanced adverse ventricular remodelling following MI [10] , a state which was reversed by the use of an AT1R blocker and as such the pathology of ACE2 deletion was attributed to the increased levels of Ang II [10] . A mounting body of evidence is forming in support of a cardioprotective role for ACE2, through the metabolism of Ang II [10, 11] , but also through the direct action of Ang-(1-7) via its own receptor, Mas [12] . Like Ang II the actions of Ang-(1-7) extend beyond vasopressor control, and for the most part appear to counteract the effects of Ang II and therefore mediate cardioprotection [13] . Ang-(1-7) reduces interstitial fibrosis [14] , myocyte hypertrophy [15] and inhibits myocyte cell growth [16] . The reduction in myocyte hypertrophy resulting from expression of Ang-(1-7) was associated with a decrease in pro-inflammatory cytokines (TNF-a and IL-6) and also a reduction in exogenous ACE transcript [17] .