Treatment of the 3XTg-AD mice with an antibody against IL-1 reduces S100B levels and results in attenuation of tau pathology and in partial reduction of certain fibrillar and oligomeric forms of Aβ (Kitazawa et al., 2011) Therefore, S100B seems to be tied to different processes related to AD pathology as in addition to its ability to promote brain inflammatory response and tau pathology (Esposito et al., 2008b) it may play roles in directly promoting amyloidogenic APP processing, as proposed by Mori et al. (2010). The gene discussed is IL1B; the disease is Alzheimer disease.