Recently two phases have been identified in the pathophysiology of sepsis: a first phase characterized by a substantial increase of the pro-inflammatory mediators including cytokines, and systemic inflammatory markers, for example, procalcitonin (PCT) and C-reactive protein (CRP), and a second phase (immunoparalysis, immunodysregulation) with the rise of anti-inflammatory mediators [4,5]. This evidence concerns the gene CRP and Sepsis.