These include generation of reactive oxygen species (ROS)/oxidative stress, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, accumulation of advanced glycated end-products (see also section on vascular dysfunction), and hyperglycemia-induced alterations in signaling by growth factors, peptides of RAAS as well as other GPCRs that are known also to transactivate EGFR (for recent reviews see Babel and Dandekar, 2021; Kenny and Abel, 2019, Forrester et al., 2016). This evidence concerns the gene EGFR and Hyperglycemia.