Events that either lead or predispose to ALI/ARDS often involve three interrelated pathophysiologic conditions: (i) increased microvascular permeability, (ii) alveolar instability reducing lung compliance, and (iii) overactive and disrupted lung inflammatory responses like interleukins (IL-1, IL-6), chemokines, tumor necrosis factor (TNF-α), oxidants (superoxide ions, hydrogen peroxide, nitric oxide), and proteases, which escalate inflammation by destroying alveolar architecture (Matuschak and Lechner, 2010). The gene discussed is TNF; the disease is acute respiratory distress syndrome.