ADT-OH and derivatives, such as ADT and ATB-346, contribute to regeneration by modulating neural progenitor cell differentiation via β-catenin/TCF7L2 [64], reducing scarring and microglial activation in SCI [65], shifting microglia to the M2 phenotype via AMPK [66], and stabilizing the BBB through NF-κB in stroke [67], while suppressing Akt/VEGF/MMP9 [68] and edema in TBI [69]. This evidence concerns the gene AKT1 and stroke disorder.