Under the influence of proinflammatory cytokines (TNF-α, IL-1, INF-γ) circulating in the blood, the adhesion molecules undergo expression both on the surface of the endothelium and on neutrophils, creating the possibility of phagocytes penetrating into the focus of infection and fulfilling the physiological role of these cells, that is, destroying the pathogen [71]. This evidence concerns the gene IL1A and infection.