The mechanism of cytochrome c oxidase depletion could involve phosphorylation of its subunit 1 [61] at an early stage of sepsis through early pro-inflammatory mediators (i.e., TNF α) in addition to its early interaction with NO [45], which leads to a lack of ROS regulation at its level [79], and consequently to oxidation and depletion of mitochondrial proteins, including ATP synthase [12] (Figure 3B). This evidence concerns the gene TNF and Sepsis.