In addition, scholars suggested that intracerebroventricularly microinjected human adipose-derived MSCs-Exos (AD-MSCs-Exos) specifically entered microglia/macrophages and suppressed their activation by inhibiting the NF-κB and MAPK signaling pathway after TBI, thereby increasing neurogenesis, suppressing neuroinflammation, reducing neuronal apoptosis, and promoting functional recovery [82]. The gene discussed is NFKB1; the disease is Alzheimer disease.