showed using an OVA murine model that not only the protein levels of RIPK2 are increased in asthma, but also, and more importantly, that the knockdown of RIPK2 via intratracheal administration of a specific siRNA ameliorates the experimental asthma phenotype including significant reductions in AHR, eosinophil recruitment, lower levels of IL4, IL5, IL13, IL33 and seric OVA-specific IgE (132). The gene discussed is AHR; the disease is asthma.