During inflammatory diseases such as sepsis and atherosclerosis, vascular endothelial cells may not be exposed to a single inflammatory mediator, rather, different inflammatory mediators such as Wnt5A and the prototypic proinflammatory prothrombotic proatherogenic IL-1β simultaneously act paracrinically on vascular endothelial cells and their crosstalk may modulate inflammatory responses in vascular endothelial cells (Pereira et al., 2008; Bhatt et al., 2012; Schulte et al., 2012; Gatica-Andrades et al., 2017; Skaria and Schoedon, 2017). This evidence concerns the gene WNT5A and atherosclerosis.