Here we aim to verify whether miR-34c in BMSC-sEVs act to attenuate lung edema via upregulating γ-ENaC expression through targeting MARCKS and activating the PI3K/AKT signal pathway subsequently; the evidence of this would provide more information that could lead to the discovery of a novel therapeutic strategy for ALI. The gene discussed is MARCKS; the disease is acute respiratory distress syndrome.