showed that TLR2, through activation of NADPH oxidse2(NOX2), can increase endothelial nitric oxide synthases(eNOS) uncoupling and total superoxide production in aortic endothelial cells, leading to impaired NO bioavailability and insufficient endothelium‐dependent vascular relaxation in type 2 diabetes mellitus (T2DM) patients and that knockdown of TLR2 can correct these pathological responses. This evidence concerns the gene CYBB and type 2 diabetes mellitus.