TMSB4X and familial Alzheimer disease: The defects of neurogenesis and increase of Aβ in fAD cerebral organoids can be rescued by treatment with thymosin beta 4 (Tβ4), the protein product of TMSB4X. Overexpression of TMSB4X in neurons via AAV-TMSB4X rescued the pathological changes and mitigated neuronal hyper-excitability in 5xFAD mice.