Ischemic and hypoxic conditions also cause GFAP release.[12, 13] The amount of brain tissue destruction directly correlates with GFAP serum concentrations.[7, 9, 10] On the other side, GFAP is not increased in mild cerebral injury not affecting the structural integrity of astrocytes.[5] Moreover, transient cerebral ischemia does not cause higher GFAP concentrations, as long as ischemic cell death and necrosis do not occur.[14] Previous studies showed that GFAP can be detected in post mortem brain specimen, both from humans and rodents. The gene discussed is GFAP; the disease is transient ischemic attack.