SOCS1 and acute respiratory distress syndrome: P-MSC-EV treatment also reduces lung injury and neutrophil infiltration and improves alveolar barrier integrity.213 BM-MSC-EVs can effectively modify macrophage responses, even with inflammatory triggers such as hypo- and hyperinflammatory ARDS plasma.214 This reprogramming was achieved through the transfer of miR-181a in BM-MSC-EVs, which led to the downregulation of phosphatase and tensin homolog (PTEN) and the increase in pSTAT5 and suppressor of cytokine signaling 1 (SOCS1).