This dependence of Alternaria intrinsic serine protease activity in driving this IL-33–mediated inflammation could underlie the potential of fungal proteases to act as TH2 adjuvants.27, 28 A recent study demonstrated that fungal-derived proteases cleave fibrinogen, which subsequently elicits allergic inflammation via TLR4 signalling,29 a mechanism that could also contribute to our observed Alternaria-specific phenotype. The gene discussed is TLR4; the disease is inflammation.