In the present study, we observed a higher copper overload in the lung tissue of experimental MA-ALI/ARDS mice by both RAC staining and ICP-MS, followed by a notable increase in the expression of SLC31A1 (a copper import transporter) and FDX1 (a key positive cuproptosis regulatory), but a significant decline in the expression of ATP7A (a copper export transporter), thereby indicating that cuproptosis could occur in the process of MA-ALI/ARDS. The gene discussed is SLC31A1; the disease is acute respiratory distress syndrome.