The present study demonstrates that ASLNC12002 regulates EMT by NR2F2/miR128-3p/Snail1 pathway and knockdown of ASLNC12002 inhibits EMT, thus indicating that ASLNC12002 may be a potential target for therapy of sepsis-induced ARDS and its related products (such as degradation residues, encoded polypeptides, etc.)have the potential to become diagnostic and prognostic biomarkers for patients with sepsis-induced ARDS. Here, SNAI1 is linked to acute respiratory distress syndrome.