1996; Fisher et al. 1995), indicating its efficacy in suppressing primary brain damage. Yet, intracisternal administration of bFGF via the ventricles did not reduce cerebral infarction (Kawamata et al. 1996). In the present study, the bFGF‐releasing dura mater was placed at the site of brain injury; hence, mechanism of action of the released bFGF should be similar to that of intrathecally administered bFGF. As mentioned above, the biological effect of intrathecally administered bFGF is likely to sustain longer than intravenously administered bFGF (Xie et al. 2015; Yang et al. 2013). The gene discussed is FGF2; the disease is brain infarction.