Interestingly, Müller glia adopted the characteristic neuroinflammatory phenotype in the context of diabetes induced-mitochondrial hyperfusion, as shown by the upregulation of intermediate filaments (i.e., Vimentin) and the release of inflammatory factors, including MCP-1 and VEGF-A (both elevated in the vitreous of DR individuals)44–46. This evidence concerns the gene VEGFA and diabetes mellitus.