Singh et al. (2016) found that the HMGB1-TLR2-MYD88 pathway was upregulated in a mouse model of acute hypoxia (AH), with marked increases in Sp1 phosphorylation and vWF levels. Further studies demonstrated that silencing TLR2 inhibited Sp1 phosphorylation and prevented Sp1 from combining with the vWF promoter, thereby reducing vWF levels as well as alleviating AH-induced insulin resistance. This suggests that hypoxia-mediated enhancement of the TLR2-Sp1-vWF pathway plays a critical role in the etiology of atherosclerosis (Singh et al., 2016). This evidence concerns the gene SP1 and atherosclerosis.