Based on these data, we envision a scenario in which retinal upregulation of IL-1β in diabetes initiates in the vascular endothelium as a direct effect of hyperglycemia, and the secreted IL-1β stimulates in an autocrine and paracrine manner endothelial and macroglia cells, which respond not only with signs of activation but also with enhanced synthesis of IL-1β, thereby magnifying the features of neuroinflammation. Here, IL1B is linked to diabetes mellitus.