NFKB1 and Hyperglycemia: [36], [38]–[41] Recently, in vitro hyperglycemic models have demonstrated the ability of hyperglycemia to induce endothelial cell dysfunction consistent with pathologies observed in T2D patients including, NFkB activation, inflammation, and reduced NO production. [39], [42]–[44] The results of this study are the first demonstration of hyperglycemia as a causative role in inhibiting angiogenesis in T2D.