CONCLUSION
Dissecting the genetic architecture will not only contribute to a better understanding of the etiology of stuttering but also facilitate the identification of new targets with implications to prevention, diagnosis and treatment. Using ES, we generated an enriched list of 14 target genes (COL4A2, COL6A3, COL6A6, ITGAX, LAMA5, ADAMTS9, CSGALNACT1, TMOD2 , HTR2B , RSC1A1 , TRPV2, WNK1 , ARSD andSPTBN5) involved in neural related pathways, in the two multiplex families studied. We propose that these 14 genes having role in signaling and transport may be putatively linked to stuttering. However in STU 65 family, a homozygous variant in NLRP11 gene and a heterozygous variant in NAGPA gene were also identified. ES in additional members and further functional validation would ensure the role of these genes in stuttering.