The development of ARDS also linked to the activation of Ang-II pathways which highly trigger-up the adaptive immunity through the excessive release of infiltrating macrophages and other pro-inflammatory mediators [22] leading to over expression of interleukins, tumour necrosis factor α (TNF-α), interferon-gamma (IFNγ), and chemokines (e.g. CXC L10, and CCL2) which results in massive cytokine storm [21,22]. This evidence concerns the gene CXCL10 and acute respiratory distress syndrome.