This mechanism may play an important role in IgE-independent mast cell mediator release in asthma, for example during EIB, and in non-atopic asthma where common aeroallergens do not appear to contribute but levels of endogenous indirect activators of TRPV4 such as tryptase are elevated [49] and also where cysLT1 receptor antagonists such as montelukast have been shown to be effective [52]. The gene discussed is TRPV4; the disease is asthma.