It is possible to hypothesize that anxious and depressive symptoms during MS may be triggered by the pathological interaction of proinflammatory molecules with specific synaptic targets and clinical studies support this hypothesis, since CSF levels of pro-inflammatory cytokines, such as interleukin-2 (IL-2), IL-1β and TNF-α, correlated with the degree of anxiety and depressive symptoms in MS patients [203]. The gene discussed is TNF; the disease is myeloid sarcoma.