It is known that TRL4 activates nuclear factor-kB (NF-kB) signaling pathways linked to the synthesis of many inflammatory proteins such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-α) and interleukins, such as interleukin-1β (IL-1β), in many human diseases, including cardiovascular diseases, diabetes, bipolar disorder and chronic fatigue syndrome [21,35,41]. This evidence concerns the gene TNF and myalgic encephalomeyelitis/chronic fatigue syndrome.