There are several possible mechanisms for this such as 1) the barrier disruption caused by HCl facilitates the egress of MCh from the airway lumen to the underlying smooth muscle, resulting in airway hyperresponsiveness, 2) edema within and around the airways that reduces the airway lumen, and 3) elevated cytokines caused by HCl, such as TNF-α, induce calcium influx into airway smooth muscle cells and lead to smooth muscle contraction (Spond et al., 2004). The gene discussed is TNF; the disease is airway hyperresponsiveness.