NFKB1 and type 2 diabetes mellitus: Since NFκB is a major regulator of pro-inflammatory cytokines, we hypothesize that the aforementioned reduction of NFκB-p65 protein levels and, as a consequence, proinflammatory cytokine TNFα expression by SS-31 is responsible, at least in part, for the lower adhesiveness of leukocytes in T2D patients through an inhibition of the cytokine-driven leukocyte-endothelial cell interaction.