We also showed, using both an OVA-induced mouse model of chronic airway inflammation25 and a house dust mite (HDM)-induced asthma model, and testing two different types of genetically MC-deficient mice, that TNFRSF14 expression specifically on MCs is necessary for the full development of multiple features of asthma pathology in mice, including plasma levels of Ag-specific IgE and IgG1 antibodies, AHR, airway inflammation and airway remodelling. The gene discussed is TNFRSF14; the disease is asthma.