IL36G and congenital rubella syndrome: IL-36α, IL-36β, and IL-36γ, which are highly expressed in the sinus mucosa of patients with chronic rhinosinusitis (CRS), can act as response elements to microorganisms and other organisms through Toll-like receptor (TLR) signaling pathways and promote CXC class chemokine production to interact with innate and adaptive immune responses in CRS [15].