 Welcome to a video highlight of our recently published paper in Human Mutation entitled Amplicant Resequencing Identified Parental Mosaicism for Approximately 10% of the novel SN1A mutations in children with Dravid syndrome. Dravid syndrome is a severe epileptic syndrome that occurs in the first year of life, characterized by its favor-sensitive multiple serotypes. Refractory and psychomotor development delay up to zero onset. The main collagen of Dravid syndrome is the alpha-1 subunit of the sodium channel SN1A. We sequenced SN1A in 363 charnet patients and identified 223 heterozygous mutations in 255 patients. PCR single sequencing of the same SN1A mutations in the parents revealed that in five families, the mutations could be identified in one of the parents as mosaic. Genomic mosaicism results from posagotic mutations occurring during development or aging which may give rise to two or more cell populations with distinct genome sequences within one individual. They may affect the somatic cells, germline cells, or both. Here we are particularly interested in genomic mosaicism affecting both the somatic cells and germline cells. We wanted to quantify the allylic fractions of the mosaic mutations in the parents. Furthermore, we wanted to find out whether any of the novel mutations were in fact inherited from parental mosaicisms undetected by Sanger sequencing. We took advantage of the next generation sequencing approach to develop a high throughput and sensitive technology for the detection and quantitation for genomic mosaicism. We developed PASM, which stands for PGM Amplicon Sequencing of Mosaicism. Here is a flow chart of PASM. Targeted PCR amplification was used to capture the genomic region around a mutation. Library preparation, emulsion PCR, and semiconductor sequencing on PGM were carried out following the manufacturer's instructions. We developed a hierarchical basing model to calculate the fractions of the mutant alleles. We validated the candidate mosaicism by ring job digital PCR and para sequencing. We qualified the allylic fraction of the five cases of parental mosaicism detected by Sanger sequencing at 13.3% to 32.6% respectively. We then detected and validated 15 more cases of parental mosaicism that were undetected by Sanger sequencing. The lowest fraction of mutant alleles detected was 1.1%, 13 out of total of 20 mutations originated from paternal mosaicism and 7 from maternal mosaicism. We identified mosaicisms with varied allylic fractions in blood, saliva, urine, hair follicle, oral epicillin, and salmon. Demonstrating that post-psychotic mutations could affect multiple somatic cells as well as germ cells. 60% of the mosaic parents did not have any epileptic symptoms. The mutant allylic fractions were significantly lower than those in mosaic parents with epileptic symptoms. Our results suggested that using more sensitive tools for detecting low-level mosaicism in parents of children with de novo mutations could allow for better informed genetic counseling. For more information, please refer to our publication in Human Mutation where contact doctors Yoo Hwa-Jung and Li Pinwei.