In the context of diabetes, it would be of interest to investigate whether: (1) pro-inflammatory stimuli (such as TNFα or LPS) known to stimulate Ninj-1 expression and oxidative stress [55]; (2) AGE products as ligands for RAGE and stimulators of oxidative and inflammatory stress [37,52]; (3) different DAMPs (including HMGB-1) known to increase the inflammatory stress and the transendothelial transport [80] can activate similar pathways as the ones in the present manuscript. This evidence concerns the gene NINJ1 and diabetes mellitus.