PRRT2 and atherosclerosis: There is an increasing consensus that increased advanced glycation end-products (AGEs) formation, activation of protein kinase C (PKC) isoforms, increased polyol pathway flux, and increased hexosamine pathway flux play vital roles in hyperglycemia-induced atherosclerosis (Brownlee, 2001; Chait and Bornfeldt, 2009; Bornfeldt and Tabas, 2011; Yuan et al., 2019).