Studies have shown that upregulation of the expression of NAD(P)H-quinone oxidoreductase proteins in mammals could significantly improve the neurological status after traumatic brain injury (TBI)21 and alleviate osteoporosis by reducing the activation of NF-κB, MAPK, and AKT signaling pathways during osteoclast formation.22 However, the same therapeutic effects have not yet been demonstrated with NAD(P)H-quinone oxidoreductase from Drynariae Rhizoma roots EVs, which is worth further study. This evidence concerns the gene AKT1 and brain injury.