During sepsis, bacterial products and proinflammatory cytokines, such as TNF-α and IL-1β, reduce the expression of L-selectin on the surface of neutrophils and stimulate the expression of β-integrins that interact with the intercellular adhesion molecule 1 (ICAM-1) and the vascular cell adhesion molecule 1 (VCAM-1) on the vascular endothelium and thereby contribute to the high affinity adhesion to the endothelium [59]. This evidence concerns the gene ICAM1 and Sepsis.