Since anti-inflammatory pyridinyl imidazole drugs such as MAPK inhibitors have been identified as putative drugs for antiinflammatory therapies [50], as have therapeutics targeting TNF-α-mediated brain inflammation [51], the data presented in this paper suggest that inhibiting such molecules (MAPK and TNF-α) may represent pharmaceutical strategies to restrict MMP-9 secretion, thereby potentially reducing morbidity associated with neurobrucellosis. The gene discussed is TNF; the disease is brain inflammatory disease.