Additionally, cells carrying the asthma risk haplotype and stimulated with 50 ng/mL IL-33 were more amenable to the antiinflammatory effects of blocking either IL1RL1 or IL-33 using monoclonal antibodies compared with the alternative haplotype, where blocking antibodies had a minimal effect on reducing NF-κB signaling (Figure 6, C and D). This evidence concerns the gene IL1RL1 and asthma.