Sustained activation of the IL-23/IL-17 axis can upregulate endothelial adhesion molecules (VCAM-1, ICAM-1), enhance neutrophil extracellular network (NETs) formation, and promote monocyte adhesion and transformation to foam cell phenotype, thereby triggering endothelial dysfunction and early lipid streak formation (11). Here, IL17A is linked to endothelial dysfunction.