The pathogenesis of ALI/ARDS involves the development oflocal and systemic cascade inflammatory responses, accompanied by the elevationof the levels of proinflammatory cytokines (TNF-α, IFN-γ, IL-6,IL-1β, GM-CSF, and G-CSF) and chemokines (CXCL10/IP10, MIP-1α, andCCL2) up to critical values, resulting in the development of multiple organfailure [14, 15, 16]. This evidence concerns the gene CCL3 and acute respiratory distress syndrome.