In fluid-induced ALI/ARDS, high shear stress generated from rapid administration of intravenous 0.9% saline solution are suggested to induce TRPV4 overactivation and subsequently result in pulmonary endothelial hyperpermeability and pulmonary edema, and fluid-induced pulmonary edema can be alleviated by knockout of TRPV4 or treatment with TRPV4 inhibitor [59]. The gene discussed is TRPV4; the disease is pulmonary edema.