Given that IL1R2 acts as a decoy receptor to antagonize the bound ligand [21], our data prompted the speculation that hypermethylation of IL1R2 in asthma and atopy negatively regulates IL1R2 expression and less decoy receptors are available to reduce the downstream pro-inflammatory response of IL1 in the presence of unchanged IL1R1 level [22, 23]. The gene discussed is IL1R1; the disease is asthma.