Dr. Tang was originally trained as a physician in China. After three years of clinical practice in neurology, Dr. Tang took a graduate program in Shanghai Jiaotong University for his MS degree. Thereafter, supported by a scholarship from the Japanese government, Dr. Tang went to Nagoya University, Japan, to conduct his Ph.D. training under the guidance of Prof. Nabeshima, a pioneer researcher in Behavioral Neuroscience. After obtaining his Ph.D. degree, Dr. Tang moved to Princeton University, USA, for his post-doctorial training. During this period of time, Dr. Tang made a significant contribution to the understanding how a gene controls learning behaviors, and this work was published in Nature (1999). This publication did create a great impact in the field as well as in the news medium, and was listed as the 4th of top ten “Best Science in 1999” by the TIME magazine. Thereafter, Dr. Tang took an assistant professorship in the Department of Psychiatry, the University of Chicago. In 2008, Dr. Tang moved to LSUHSC as an associate professor in the Department of Cell Biology and Anatomy, and in the end of 2015, Dr Tang was appointed as an executive director of Guangzhou Institute of Pediatrics, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, China, where he is currently continuing his leadership in this Institute. Up to now, Dr. Tang obtained more than 18 grants, including from USA and China. The total amount of direct cost reached up to11,000,000 US dollar. Up to now, Dr. Tang has published more than 66 papers, including those published in top tier journals, such as Science, Nature, Cell, PNAS etc. Up to now, the citation number of his publications has reached up to nearly 10,000 times. Currently, the major research programs in Dr. Tang’s Lab include 1) behavioral genetics, with a focus on genetic basis of autism and translational significance in early diagnosis of autism; 2) genetic basis of rare disease and gene therapy; 3) genetically modified stem cell engineering and its clinical applications. Representative publications (From more than 66 papers, and up to now, the total citation number is over 9,000 times) 1. Chen WX, et al (2022) De novo mutations within metabolism networks of amino acid/protein/energy in Chinese autistic children with intellectual disability. Hum Genomics E-pub. 2. Zou F, et al (2021) The CD39 + HBV surface protein-targeted CAR-T and personalized tumor-reactive CD8 + T cells exhibit potent anti-HCC activity. Mol Ther 29:1794-807. 3. Wang X, et al (2019) Maternal Diabetes Induces Autism-Like Behavior through Hyperglycemia-Mediated Persistent Oxidative Stress and Suppression of Superoxide Dismutase 2. Proc Natl Acad Sci USA 116: 23743-52. 4. Jiang X, et al (2019) A novel GTPCH deficiency mouse model exhibiting tetrahydrobiopterin-related metabolic disturbance and infancy-onset motor impairments. Metabolism 94:96-104. 5. Hao Z, et al (2019) Maternal exposure to triclosan constitutes a yet unrecognized risk factor for autism spectrum disorders. Cell Res 29: 866-69. 6. Yang H, et al (2015) Protein phosphatase-1 inhibitor-2 is a novel memory suppressor. J Neurisci 35: 15082-7. 7. Cheng L, et al (2014) Expression of the G72/G30 gene in transgenic mice induces behavioral changes. Mol Psychiatry 19: 175-83. 8. Chen R, et al (2013) Δ(9)-THC-Caused Synaptic and Memory Impairments Are Mediated through COX-2 Signaling. Cell 155:1154-65. 9. Joseph A, et al (2013) A temporal association of elevated CCKergic tone and adolescent trauma is critical for the development of PTSD-like behavior in adult mice. Proc Natl Acad Sci USA 110: 6589-94. 10. Chen R, et al (2012) Monoacylglycerol lipase contributes to pathogenesis of Alzheimer’s disease. Cell Rep 2: 1329-39. 11. Chen Q, et al (2010) Bi-directional effect of cholecystokinin receptor-2 overexpression on stress-triggered emotional memory and anxiety in the mouse. PLoS ONE 5: e-15999. 12. Im HI, et al (2009) Dephosphorylation of eEF-2 in the hippocampus promotes protein synthesis for memory consolidation. PLoS ONE 4: e7424. 13. Chen Q, et al (2008) Adult neurogenesis is functionally associated with Alzheimer’s disease-like neurodegeneration in the mouse. Neurobiol Dis 29: 316-326. 14. Lazaroy O, et al (2005) Environmental enrichment reduces a-b levels and amyloid deposition in transgenic mice. Cell 120: 701-713. 15. Feng R, et al (2001) Deficient neurogenesis in presenilin-1 forebrain knockout mice prevents clearance of hippocampal memory traces. Neuron 32: 911-926. 16. Shimizu E*, Tang YP*, et al (2000) NMDA receptor-dependent synaptic reinforcement as a crucial process for memory consolidation. Science 290:1170-1174. 17. Rampon C*, Tang YP*, et al (2000) Enrichment induces structural changes and recovery from nonspatial memory deficits in CA1 NMDAR1-knockout mice. Nat Neurosci 3: 238-244. 18. Tang YP, et al (1999) Genetic enhancement of learning and memory in mice. Nature 401: 63-69. *, these authors contributed equally