The synaptogenic function of C3a-C3aR signaling in the post-stroke adult brain was further supported by the finding that mice that received daily intranasal treatment with C3a for 14 to 21 days starting 7 days after ischemia induction had higher density of pre-synaptic terminals and faster functional recovery that was sustained 4 weeks after cessation of the treatment [89]. The gene discussed is C3; the disease is stroke disorder.