Another research conducted on umbilical vein endothelial cells (HUVEC) showed that accumulation of endogenous Alu RNA during hyperglycemia provoked oxidative stress and dysfunction in these cells, by impeding the expression of superoxide dismutase 2 (SOD2) and endothelial nitric oxide synthase (eNOS) at transcription and translation levels via the NFκB signaling pathway. Here, SOD2 is linked to Hyperglycemia.