Editing Controversies in autism (section)

==Genetics==
{{further|Heritability of autism}}
The role of genetic influence on ASD has been heavily researched over the past few years. ASD is considered to have polygenic traits since there is not a single risk factor, but multiple ones.<ref name=":12">{{cite journal | vauthors = Robinson EB, Neale BM, Hyman SE | title = Genetic research in autism spectrum disorders | journal = Current Opinion in Pediatrics | volume = 27 | issue = 6 | pages = 685–91 | date = December 2015 | pmid = 26371945 | pmc = 4650984 | doi = 10.1097/MOP.0000000000000278 }}</ref>

Multiple twin and family studies have been conducted in order to observe any genetic influence in diagnosing ASD. The chance of both twins having ASD was significantly higher in identical twins than fraternal twins, concluding that ASD is heritable.<ref name=":02">{{cite journal | vauthors = Bourgeron T | title = Current knowledge on the genetics of autism and propositions for future research | journal = Comptes Rendus Biologies | volume = 339 | issue = 7–8 | pages = 300–7 | date = 1 July 2016 | pmid = 27289453 | doi = 10.1016/j.crvi.2016.05.004 | doi-access = free }}</ref>  A reoccurring finding is that ''de novo'' (new mutation) [[Copy-number variation|copy number variants]] (CNVs) are a primary cause of ASD&nbsp;– they alter synaptic functions; [[Germline mutation|germ line mutations]] can produce ''de novo'' CNVs.<ref>{{cite journal | vauthors = Ronemus M, Iossifov I, Levy D, Wigler M | title = The role of de novo mutations in the genetics of autism spectrum disorders | language = En | journal = Nature Reviews. Genetics | volume = 15 | issue = 2 | pages = 133–41 | date = February 2014 | pmid = 24430941 | doi = 10.1038/nrg3585 | s2cid = 9073763 }}</ref> These mutations can only be passed on to offspring; this explains the phenomenon that occurs when the child has symptoms of ASD, but the parents have no symptoms or history of ASD. ''De novo'' variants differ from person to person, i.e. one variant can cause ASD in one person, whereas another person would need multiple variants to cause the same disorder.<ref name=":02" /> Loss of function variants occur in 16-18% of ASD diagnoses, which is nearly double the normal population.<ref name=":12" /> These loss of function variants reduce function in the protein [[neurexin]], which connects neurons at the synapse and is important for neurological development; [[Deletion (genetics)|deletion mutations]] of neurexin are also very common in people with autism, as well as other neurological disorders like [[schizophrenia]], [[bipolar disorder]], and [[Attention deficit hyperactivity disorder|ADHD]].<ref>{{cite journal | vauthors = Chen J, Yu S, Fu Y, Li X | title = Synaptic proteins and receptors defects in autism spectrum disorders | journal = Frontiers in Cellular Neuroscience | volume = 8 | pages = 276 | date = 11 September 2014 | pmid = 25309321 | pmc = 4161164 | doi = 10.3389/fncel.2014.00276 | doi-access = free }}</ref>

There is also controversy over the [[Nature versus nurture|Nature vs. Nurture]] debate. According to family studies, genetic and environmental factors have an equal influence on risk of ASD.<ref name=":02" />