In chemically induced ALI/ARDS, these chemical stimuli (hydrochloric acid and chlorine gas) can increase endogenous TRP channel agonists (e.g., N-acylamides), which can activate TRPV4, and both the knockout of TRPV4 and treatment with TRPV4 inhibitors (e.g., GSK2220691 and GSK2337429A) can decrease immune cell infiltration, reduce oxidative mediator production and inflammatory cytokine release, prevent epithelial and endothelial barrier function, and improve lung function [37, 113]. The gene discussed is TRPV4; the disease is acute respiratory distress syndrome.