The actions of PPS reported in other studies provided the rationale for its use in ARDS, which involved anti-inflammatory actions mediated via inhibition of NF-κB activation (23–26); inhibition of complement (C3, C3Bb and C5b9) mediated tissue injury (27); inhibition of endothelial cell activation (28); and adverse tissue remodeling by inhibiting fibroblast growth factor-2 (FGF-2) (29) and matrix metalloproteinases (MMPs), ADAMTS-4 (30–32) and elastase (33). The gene discussed is FGF2; the disease is acute respiratory distress syndrome.