Two major pathways with opposite effects involve growth factors during ARDS: tyrosine kinase receptor mediation (e.g., KGF, HGF, FGF, and VEGF) and serine-threonine kinase receptors such as TGF-β1, which tend to have opposed effect on the upregulation that occurs when the tyrosine kinase receptor pathway is involved [85, 191, 192]. The gene discussed is HGF; the disease is acute respiratory distress syndrome.