Although the exact mechanisms by which TLRs modulate the evolution of ischemic brain injury have not been fully elucidated, pharmacological inhibition of TLR2 and TLR4 and/or blockade of some of their endogenous ligands (i.e., cellular fibronectin or heat shock protein 60), represent promising therapeutic options, effective in reducing the inflammatory response to stroke injury (Brea et al., 2011). This evidence concerns the gene TLR4 and Stroke.