The release of HMGBI, a TLR2 agonist, from the dead glioma cells stimulated TLR2 (Foldi, 1999), and in combination with the local expression of the DC growth factor Fms-like tyrosine kinase 3 ligand (Flt3L) (Maraskovsky et al., 1996; Pulendran et al., 1997), led to expansion and activation of DCs resulting in the production of inflammatory cytokines TNF-α and IL-6 (Curtin et al., 2009) necessary to initiate an effective anti-glioma immune response (Ali et al., 2004). The gene discussed is TLR2; the disease is glioma.