However, due to the complex pathophysiology of stroke and the vast spectrum of molecular events triggered by the initial insult, UCH-L1 and GFAP cannot be sufficient and it will be necessary to broaden our arsenal to cover other significant pathophysiological mechanisms that come into play including inflammation, oxidative stress, axonal injury and remodeling and molecular reorganisation of membrane and extracellular-matrix proteins. This evidence concerns the gene GFAP and stroke disorder.