In particular, it would seem that the hyperproduction of insulin in patients with diabetes and the consequent activation of the PI3K/Akt/mTOR pathway would lead to a stimulation of the inflammatory response, favoring the release of pro-inflammatory cytokines, such as tumor necrosis factor (TNF) and interleukin-6 (IL-6) [13,14,15,16]. Here, AKT1 is linked to diabetes mellitus.