Editing Glaucoma (section)

===Family history and genetics===
Positive family history is a risk factor for glaucoma. The relative risk of having primary open-angle glaucoma is increased about two- to four-fold for people who have a sibling with glaucoma.<ref name=yanoff>{{cite book| vauthors = Yanoff M, Duker JS |title=Ophthalmology|year=2009|publisher=Mosby Elsevier|isbn=978-0-323-04332-8|page=1096|edition=3rd}}</ref> Glaucoma, particularly primary open-angle glaucoma, is associated with [[mutation]]s in several [[gene]]s, including ''[[MYOC]], ASB10, [[WDR36]], [[Neurotrophin-4|NTF4]]'', ''[[TANK-binding kinase 1|TBK1]]'',<ref name="OMIM137760">{{OMIM|137760|Glaucoma, Primary Open Angle; POAG}}</ref> and ''[[RPGRIP1]].''<ref>{{cite journal | vauthors = Fernández-Martínez L, Letteboer S, Mardin CY, Weisschuh N, Gramer E, Weber BH, Rautenstrauss B, Ferreira PA, Kruse FE, Reis A, Roepman R, Pasutto F | display-authors = 6 | title = Evidence for RPGRIP1 gene as risk factor for primary open angle glaucoma | journal = European Journal of Human Genetics | volume = 19 | issue = 4 | pages = 445–451 | date = April 2011 | pmid = 21224891 | pmc = 3060327 | doi = 10.1038/ejhg.2010.217 }}</ref> Many of these genes are involved in critical cellular processes that are implicated in the development and progression of glaucoma, including regulation of intraocular pressure, retinal ganglion cell health, and optic nerve function.<ref name="pmid28505344">{{cite journal| author=Wiggs JL, Pasquale LR| title=Genetics of glaucoma. | journal=Hum Mol Genet | year= 2017 | volume= 26 | issue= R1 | pages= R21–R27 | pmid=28505344 | doi=10.1093/hmg/ddx184 | pmc=6074793 }} </ref> Normal-tension glaucoma, which comprises 30-90% of primary open-angle glaucoma (depending on ethnic group),<ref name="pmid26886116">{{cite journal| author=Kim KE, Park KH| title=Update on the Prevalence, Etiology, Diagnosis, and Monitoring of Normal-Tension Glaucoma. | journal=Asia Pac J Ophthalmol (Phila) | year= 2016 | volume= 5 | issue= 1 | pages= 23–31 | pmid=26886116 | doi=10.1097/APO.0000000000000177 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26886116  }}, (review) (open access).</ref> is also associated with genetic mutations (including ''[[OPA1]]'' and ''[[Optineurin|OPTN]]'' genes).<ref>{{OMIM|606657|Glaucoma, Normal Tension, Susceptibility to}}</ref>

Additionally, some rare genetic conditions increase the risk of glaucoma, such as [[Axenfeld–Rieger syndrome|Axenfeld-Rieger syndrome]] and [[primary congenital glaucoma]], which is  associated with mutations in ''[[CYP1B1]]'' or ''[[LTBP2]].''<ref name=":5">{{Cite journal |last1=Badawi |first1=Abdulrahman H. |last2=Al-Muhaylib |first2=Ahmed A. |last3=Al Owaifeer |first3=Adi Mohammed |last4=Al-Essa |first4=Rakan S. |last5=Al-Shahwan |first5=Sami A. |date=2019-10-01 |title=Primary congenital glaucoma: An updated review |journal=Saudi Journal of Ophthalmology |volume=33 |issue=4 |pages=382–388 |doi=10.1016/j.sjopt.2019.10.002 |pmid=31920449 |pmc=6950954 |issn=1319-4534}}</ref> They are inherited in an autosomal recessive fashion.<ref name=":5" /> Axenfeld-Rieger syndrome is inherited in an autosomal dominant fashion and is associated with ''[[PITX2]]'' or [[Forkhead box C1|''FOXC1'']].<ref>{{Citation |last1=Zamora |first1=Edgar A. |title=Axenfeld-Rieger Syndrome |date=2023 |url=http://www.ncbi.nlm.nih.gov/books/NBK538504/ |work=StatPearls |access-date=2023-09-22 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=30860739 |last2=Salini |first2=Baby}}</ref>