Multiple fibrotic diseases such as acute lung injury (ALI), scleroderma, and idiopathic pulmonary fibrosis (IPF) share many pathophysiological features, including a pro-inflammatory stimulus leading to a rapid release of IL-8 and IL-6 by alveolar macrophages that further attract neutrophils, causing alveolar and endothelial injury [1] and ultimately resulting in high mortality rates. This evidence concerns the gene IL6 and pulmonary fibrosis.