PRRT2 and atherosclerosis: The building of advanced glycation end products (AGEs) which is mainly determined by the level of glucose and time of exposure, the induction of hyperglycaemia induced oxidative stress, hyperglycaemia mediated inflammation through cytokines including activation of monocytes and adipocytes, the activation of the hexosamine pathway and the regulation of proteinkinase C (PKC) activity are interacting and engaging in the pathogenesis of atherosclerosis as described above.