For instance, in chemical-induced ALI/ARDS, several chemical stimuli (e.g., hydrochloric acid and chlorine) increase the production of endogenous TRPV4 agonists (e.g., N-acylamides) which can excessively activate TRPV4 and induce pulmonary edema, protein leakage, and immune cell filtration in the lungs, but the exact cell-type contributing to the effect of TRPV4 are needed further investigation [37]. The gene discussed is TRPV4; the disease is acute respiratory distress syndrome.