Hyperglycemia and inflammatory signalling activate NOX isoform—particularly NOX2 in vascular endothelial cells—leading to excess ROS production.[33, 34, 35] Beyond oxidative damage, ROS act as second messengers that promote EndMT through canonical fibrotic/inflammatory cascades, including TGF‐β/SMAD, Wnt/β‐catenin, NF‐κB, and MAPK.[36, 37, 38] Consistent with this framework, our transcriptome data show that NOX2 deletion downregulated EndMT pathway genes while restoring endothelial‐identity and vessel‐stability programs. Here, CYBB is linked to Hyperglycemia.