NFKB1 and Hyperglycemia: Mechanistically, high glucose (HG) levels, deriving from diabetes-associated chronic hyperglycaemia, induce inflammation via a variety of mechanisms, including ROS accumulation, pro-inflammatory MAPK cascade signalling, and NF-κB activation [9], which promotes the transcription of pro-inflammatory cytokines and adhesion molecules and related monocyte activation [6,10,11].