Given the multiple effects of Th2-associated cytokines on airway inflammation[7-11] and remodeling[12-14], it was unclear whether IL-4 and IL-13 would stimulate HLA-G expression and abundance in airway epithelial cells that would be counter-regulatory to inflammation, or whether, as promoters of airway inflammation, IL-4 and IL-13 would actually downregulate HLA-G expression. The gene discussed is IL4; the disease is inflammatory response.