The decrease of SIRT6 deacetylase activity in response to pressure overload or hypertrophic stimuli such as angiotensin II, isoprenaline and PE contributes to the pathogenesis of cardiac hypertrophy, although its expression is not altered (Cai et al., 2012; Yu et al., 2013; Lu et al., 2016; Shen et al., 2016; Zhang et al., 2016). This evidence concerns the gene SIRT6 and cardiac hypertrophy.