The biological relevance of H3 acetylation in p66shc expression was further supported by the observation that the overexpression of one member of class III histone deacyltransferase (HDAC) SIRT1 inhibits hyperglycaemia-induced p66shc expression, improves endothelial function, and reduces oxidative stress markers [35] A close connection between p66shc, SIRT1, and tumour transcription factor p53 [25, 36, 37] has been also reported, which supports the crucial role that the epigenetic mechanism plays in dictating cell fate, predominantly in the vascular system. Here, SIRT1 is linked to Hyperglycemia.