 Dr. Hing Miao, Director and Professor of the Institute of Neuroscience, Wanzhou Medical University. The paper I want to talk today is about a newly established SN1A gene mutation database and the role of functional alterations in determining the pathogenicity of the mutations. SN1A gene, which includes the alpha subunit of S1.1 is one of the most clinically relevant genes and is potentially associated with epilepsy, autism, and familial migraine. This database included more than 1,000 mutations with special sections on functional studies and inherited mutations. Based on the information from this database, we analyzed the relationships among genotypes, functional alterations, and phenotypes. From the genotype's phenotype point of view, we used the missing mutations which do not cause gross protein formation as in index. It was displayed that mined phenotypes were more frequently associated with missing mutations, suggesting correlations between impairment and pathogenicity. Practically, in contrast to genotype, functional alteration, phenotype in brief, is more directly linked to phenotype. Therefore, an important aspect of this type is to analyze the correlation between genotype and phenotype, phenotype and phenotype. The four homologous domains contain voltage sensors and pore-forming regions which form this alpha subunit of S1.1. For analysis, we classified the electrical physiological changes of the channel into six categories, including loss of function, partial loss of function, gain and loss of function, decreased usability, gain of function, and increased usability. Regarding genotype-phenotype relationship, it is found that missing mutations located in the pore region result in loss of function mostly and partial loss of function occasionally. While missing mutations located in the surface of the channel may need to increase visibility, gain of function, and also loss of function of different degrees. Tracating mutation occurred at the C-terminal, may produce small sodium current. While those located in the proximal part may cause complete loss of function. Regarding phenotype-phenotype correlation, it is demonstrated that why phenotype like GIFS-PRAS are associated with mined functional defects. Whereas severe phenotype like SMEI are more frequently associated with complete loss of function. It is found that there is a negative correlation between the familial instance and the phenotype severity, and incomplete penetrance was associated with missing and split site mutations, but not tracations or genomic rearrangements suggested clinical genetic concerning applications. From the data presented, we might find that ACM-1A mutation varying in pathogenicity that are corrected with phenotype severity and inheritance. When the pathogenicity of a mutation is evaluated, the possible functional consequence should be considered besides the nature of the mutation. The analysis presented in this paper is expected to be an example to exploring the relationships among genotype, phenotype, and phenotype. My colleagues and I will continue to update the information on ACM-1A mutation and make this database a really useful tool for clinical diagnosis and research. Thank you.