After the initial inflammation, HCl elicits a persistent profibrotic response, mediated by transforming growth factor-β (TGF-β) that has been related clinically to chronic conditions such as reactive airway dysfunction syndrome (RADS) [3,4], asthma-like conditions [5,6] and pulmonary fibrosis [7,8]. This evidence concerns the gene TGFB1 and pulmonary fibrosis.