RAC1 and infarction: In the ischemic stroke mouse model, it was discovered that overexpressing Ras-related C3 botulinum toxin subtype 1 (Rac1) increased peripheral cell protein levels and blood vessel density around the infarction, and that inhibiting Rac1 prevented the production of ERK1/2 and CREB, which then prevented nerve regeneration and nerve function recovery (Bu et al., 2019).