Hence, we hypothesized that sepsis molecules (LPS, cytokines, and some viable bacteria) pass through the damaged BBB and upregulate miR370-3p in brain cells, partly through the activation of TNF-α receptor (TNFR) and TLR-4 by TNF-α and LPS, respectively, that enhance mitochondrial injury (Figure 10). This evidence concerns the gene TNFRSF1A and Sepsis.