Subsequently, they demonstrated that within a model of TNF-α-induced endothelial dysfunction, IL-35 exhibited beneficial effects on EC proliferation and angiogenesis, suppression of apoptosis, enhancement of secretion of IL-10 and TGF-β, inhibition of IL-12 secretion, and attenuation of NF-κB and IκBα phosphorylation through the induction of macrophage polarization toward the M2 phenotype, ultimately resulting in enhanced endothelial function [9]. Here, NFKB1 is linked to endothelial dysfunction.