A generalized increase in oxidative stress (augmented ROS and NO production) is observed when microglia are exposed to diabetes-related conditions, accompanied by the activation of several pathways, comprising inflammatory pathways (NF-κB and NLRP3 inflammasome), oxidative stress-related pathways (HIF-1α), mitogen-activated protein kinases responding to growth factors (MEK/ERK), inflammatory cytokines (p38) and stress (JNK), the AGE/RAGE pathway, as well as the Akt/mTOR pathway, involved in regulating the cell cycle and also metabolic reprogramming. This evidence concerns the gene AKT1 and diabetes mellitus.