Since the use of humanized anti-interleukin-6 receptor antibody (tocilizumab) has been identified as a putative treatment for inflammatory encephalopathies involving neurological symptoms (77–79), the data presented in this paper suggest that the use of such a therapeutic approach might represent a medical strategy to restrict IL-6 signaling, possibly reducing the symptoms associated with neurobrucellosis or other neurological diseases in which the phagocytic activation of microglia is involved. The gene discussed is IL6; the disease is nervous system disorder.