The reactive oxidative species derived may then initiate carcinogenesis by modifying the apoptotic responses, as well as disrupting cell anchoring sites and increasing angiogenesis.57,58 In addition, studies have shown that hyperglycaemia also indirectly activates endothelial growth factor receptor (EGFR) via the Rho family GTPase Rac1 and cell division control protein 42 homolog (Cdc42), which then stimulates the cell proliferation, thus providing another mechanistic link between hyperglycaemia and tumorigenesis.59 This evidence concerns the gene EGFR and Hyperglycemia.