Elevated NLR reflects both the neutrophilia of inflammation (mediated by arachidonic acid metabolites and platelet-aggregating factors, cytotoxic oxygen-derived free radicals, and hydrolytic enzymes) [37] and relative lymphopenia, suggesting a deeper imbalance in the immunologic response, an increased expression of T helper 17 over regulatory T cells, and the activation of the interleukin-17 axis, which in turn is associated with vascular dysfunction, the progression of atherosclerosis, and vascular events [38,39]. This evidence concerns the gene IL17A and lymphopenia.