It is hypothesized that through preconditioning of the myocardium by endothelial dysfunction with impaired vasodilation, decreased availability of nitrous oxide, and increased vasoconstriction, there is an increase in endothelin-1, interleukin-6 (IL-6), interleukin-8 (IL-8), programmed cell death-ligand 1 (PD-L1), and tumor necrosis factor–alpha (TNF-α).1 This evidence concerns the gene CXCL8 and endothelial dysfunction.