During sepsis, bacterial products and pro‐inflammatory cytokines such as TNF‐α and IL‐1β promote the shedding of l‐selectin and stimulate the expression of β‐integrins on the cell surface of neutrophils, which interact with intercellular adhesion molecule‐1 (ICAM‐1) and vascular cell adhesion molecule‐1 (VCAM‐1) on the vascular endothelium and promote high‐affinity adhesion with the endothelium 23. The gene discussed is TNF; the disease is Sepsis.