Given that hyperglycaemia-induced chronic inflammation is one of the drivers of diabetic complications [3, 20] and STING has been reported to mediate innate host immunity through downstream inflammatory pathways such as IRF3/NF-κB signalling [17], we hypothesized that STING activation could mediate diabetes-induced aortic endothelial cell injury via the IRF3/NF-κB inflammatory signalling pathway. Here, NFKB1 is linked to diabetes mellitus.