It has been shown that [15] IL-36α, IL-36β and IL-36γ stimulate nasal mucosal vascular endothelial cells to cause increased permeability in patients with CRS, while in AR, an inflammatory disease of the nasal mucosa with a similar inflammatory pattern, IL-36α may also cause nasal congestion by acting on nasal mucosal vascular endothelial cells to increase vascular permeability, exudate plasma and inflammatory substances, and form local mucosal edema. Here, IL36G is linked to congenital rubella syndrome.