Endothelial oxidative stress in DM also derives from Ras-related C3 botulinum toxin substrate 1 (RAC1) and T cell lymphoma invasion and metastasis (TIAM1)-dependent activation of NOX2 [65] and diacylglycerol (DAG)/protein kinase C (PKC)-dependent phosphorylation and stimulation of the NOX activator p47phox [66]. Here, RAC1 is linked to T-cell non-Hodgkin lymphoma.