Several genes have been associated with dyslexia, including DCDC2 and KIAA0319 on chromosome 6, and DYX1C1 on chromosome 15. Gene–environment interaction
The contribution of gene–environment interaction to reading disability has been intensely studied using twin studies, which estimate the proportion of variance associated with a persons environment and the proportion associated with their genes. Both environmental and genetic factors appear to contribute to reading development. Studies examining the influence of environmental factors such as parental education and teaching quality have determined that genetics have greater influence in supportive, rather than less optimal, environments. However, more optimal conditions may just allow those genetic risk factors to account for more of the variance in outcome because the environmental risk factors have been minimized.As environment plays a large role in learning and memory, it is likely that epigenetic modifications play an important role in reading ability. Measures of gene expression, histone modifications, and methylation in the human periphery are used to study epigenetic processes; however, all of these have limitations in the extrapolation of results for application to the human brain. Language
The orthographic complexity of a language directly affects how difficult it is to learn to read it. : 266  English and French have comparatively "deep" phonemic orthographies within the Latin alphabet writing system, with complex structures employing spelling patterns on several levels: letter-sound correspondence, syllables, and morphemes. : 421  Languages such as Spanish, Italian and Finnish primarily employ letter-sound correspondence—so-called "shallow" orthographies—which makes them easier to learn for people with dyslexia.
X-linked complicated corpus callosum dysgenesis is a genetic disorder characterized by dysplasia, hypoplasia or agenesis of the corpus callosum alongside variable intellectual disability and spastic paraplegia. Only 13 cases (all male) have been described in medical literature. Transmission is X-linked recessive. It is the mildest subtype of L1 syndrome.This condition differs from other L1 syndromes due to the fact that neither hydrocephalus, adducted thumbs, or speech difficulties are common in patients with the condition. Genetics
This condition is caused by X-linked recessive mutations in the L1CAM gene, located in the long arm of the X chromosome. Mutations involved in the milder variants of L1 syndrome (including X-linked complicated corpus callosum dysgenesis) usually work by changing the L1 protein structure. Cases
The following list comprises all cases of X-linked complicated corpus callosum dysgenesis described in medical literature (from OMIM):
1964: Menkes et al. describes 5 males from 4 sibships of a 2-generation American family. The males (all infants) had partial corpus callosum agenesis, severe intellectual disabilities, developmental delays, and epilepsy. The disorder first manifested right after birth, with recurrent seizures occurring hours after it. Out of these 5 babies, 3 had died. Post-mortem examination of one of the dead infants revealed chemical and anatomical abnormalities. 1983: Kaplan et al. describes 2 males from a 2-generation Canadian family. The proband was a 2 year old male, the first-born child of healthy, non-consanguineous Ashkenazi Jewish parents in their mid-20s, his pregnancy was uneventful (besides slight vaginal bleeding experienced by the mother sometime during her first three months of pregnancy).