Impaired bone healing observed in individuals with T2DM is a multifactorial phenomenon, affecting all stages of bone repair and mediated by numerous initiators, including hyperglycaemia, chronic inflammation, oxidative stress, advanced glycation end products (AGEs), polyol pathway, high protein kinase C (PKC) activity and hexosamine biosynthesis pathways; which abrogate bone healing and angiogenic processes [(8, 10–15); summarised in Figure 1]. This evidence concerns the gene PRRT2 and Hyperglycemia.