Furthermore, during the acute phase of ARDS, C5 exhibited a protective and anti-inflammatory role through regulating matrix metalloproteinases (MMP) and cell migration, while C5 displayed a detrimental effect during the chronic phase of ARDS likely via increasing expression of fibrogenic transforming growth factor beta1 (TGF-β) and MMP-3, revealing that C5 plays opposing roles in both inflammation and lung tissue repair (243). The gene discussed is TGFB1; the disease is acute respiratory distress syndrome.