Overexpression of SOCS-1 inhibits tumor necrosis factor-α (TNF-α) production and signal transducer and activator of transcription-3 (STAT-3) activation in LPS-induced ALI and represses immune cell accumulation, lung edema, and alveolar dysfunction induced by hyperoxia [33,34]. This evidence concerns the gene SOCS1 and acute respiratory distress syndrome.