Nassini et al. 10 subsequently showed in a rodent model that systemic administration of therapeutic doses of paracetamol led to generation of its electrophilic and reactive metabolite in the lung which, in turn, caused neurogenic airway inflammation through activation of TRPA1; they proposed that this mechanism might explain the epidemiological link between paracetamol exposure and asthma in humans. The gene discussed is TRPA1; the disease is asthma.