In addition, Yang et al. provided speculation about the tissue of origin, suggesting that MSC-derived exosomal miR-144-5p modulates vascular endothelial injury [41] and improves the rat ovarian function after chemotherapy-induced ovarian failure by targeting the Akt/phosphatase and tensin homolog pathway [42], which indicates an association between increased MSCs and the expression of miR-144-5p in the TBI + RP mice. Here, AKT1 is linked to ovarian dysfunction.