This activation leads to the rapid release of cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and interleukin-18 (IL-18), driving systemic inflammation and leading to endothelial dysfunction, tissue damage, and increased vascular permeability [11]. This evidence concerns the gene IL18 and endothelial dysfunction.