Recruitment of eosinophils in CRSwNP is controlled by the local elevation of cell surface adhesion molecules, including P-selectin, β1 integrins, such as VLA-4, and β2 integrins, interacting with their respective counter-ligands expressed on inflamed endothelium of the sinus mucosa such as P-selectin ligand [CD162], VCAM-1, and ICAM-1 induced by IL-4 and IL-13 [56,84]. The gene discussed is IL13; the disease is chronic rhinosinusitis with nasal polyps.