Neuroinflammation is involved in the pathogenesis of mood disorders, as indicated by the post-mortem detection of increased protein and mRNA levels of interleukin 1β (IL-1β), interleukin 1 receptor, myeloid differentiation factor 88 (MyD88), nuclear factor-kappa B (NFκB) subunits and astroglial and microglial markers (glial fibrillary acidic protein, GFAP; inducible nitric oxide synthase, iNOS; c-fos, and CD11b) in the frontal cortex of BSD patients (110, 111). The gene discussed is GFAP; the disease is mood disorder.