Based on these data, and on the observation that treatment with miR-1281 resulted in the increase in both VEGFA mRNA abundance and VEGFA promoter-driven Luc activity in HUVEC cells, it can be speculated that increased release of miR-1281 by epithelial retinal cells in instances of chronic glucose excess, such as in diabetes, might play a pathogenetic role in DR through the activation of VEGFA protein production from adjacent endothelial cells, thereby inducing VEGFA-mediated neoangiogenesis and vascular damage of retinal vessels. This evidence concerns the gene VEGFA and diabetes mellitus.