Finally, in diabetic patients, it is hypothesised that myocardial kinases β isoform of protein kinase C (PKCβ), which is preferentially overexpressed in diabetic myocardium accompanied with increased upregulation of pro-oxidant enzyme NAPH oxidase, that is a major upstream moderator of oxidative stress and that inhibition of PKCβ can attenuate myocardial hypertrophy (54). The gene discussed is PRKCB; the disease is cardiac hypertrophy.