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C-maf inducing protein and ATPase Secretory Pathway Ca Transporting 2
[11]
These additional and closely related genes are likely to contribute to vocal learning . Applying a positional
fine-mapping approach, which required a GWAS study followed by targeted high-density association
research, two genes were implicated in language capacity: the c-maf-inducing protein (CMIP) and the
[120]
calcium-importing ATPase, type 2C, limb 2 (ATP2C2) . GWAS analysis in these families revealed a strong
and consistent linkage to locus 16q24 with the non-word repetition test. In other tissues, CMIP is involved
in a cascade of cell signaling, such as the T-cell pathway and in the binding of phospholipids. ATP2C2
hydrolyzes ATP and is part of a pathway responsible for transporting divalent ions to the Golgi apparatus,
such as calcium [113] . Linkage analysis and subsequent directed association analyses have suggested that
CMIP and ATP2C2 relate to language disorders (especially non-word repetition) and phenotypic measures
well characterized in these disorders. Although both molecules express in the brain, their functions are still
poorly understood. These genes implicate a significant association with short-term memory. Considering
that a relationship between wordless repetition test performance and short-term memory exists, ATP2C2
and CMIP can provide a biological link between memory-related pathways and language acquisition. The
fact that neither ATP2C2 nor CMIP have been identified as downstream targets of FOXP2 suggests that the
eventual combination of information from convergent research pathways will allow the characterization of
overlapping and interacting neurological systems that serve for language acquisition. Although the linkage
to these genes has documented in subsequent studies, their association with DLD has not been replicated yet.
ATP2C2 has also proved to be linked to attention deficit hyperactivity disorder (ADHD) [121,115] .

Other genes potentally associated with developmental language disorder
FOXP1 and KIAA0319 genes appear to be involved in DLD [122] . A haploinsufficiency in SETBP1 (locus 18q12)
is a factor implicated in CAS, but also in language impairment, responsible for interacting with an oncogene
[125]
implicated in DNA replication [123,124] . Other genes potentially related to language skills are ABCC13 , FLNC,
RBFOX2 [126] , and ROBO2 [127] . GWAS studies have highlighted risk variants in NDST4, ZNF385D, COL4A2 [128] ,
and NOP9 [129] . Other studies involve rare genetic events that may have greater penetrance. Also, the coding
variants within NFXL1 confer a higher risk for DLD within a complex genetic mode [130] . A study conducted
[117]
by Centanni et al. evaluated 15q11.2 as a region of susceptibility for SLD, finding two deletions in seven
patients with CAS but none in 8 SLI. The main limitation of this study was the small number of patients
(8 subjects). In a report looking for rare copy number variants in 58 subjects and their relatives, deletions
were found on chromosome 16p11.2 in 3.4% of the probands. Other detected deletions were identified in
18p11.32-p11.22 and Xp22.31-p22.33 loci. Although the proportion is low, it should be noted that this locus
overlaps with other neurodevelopmental disorders [131] . Several other minor reports exist, such as a balanced
t(10;15) translocation in a male patient with developmental language disorder [132] . This last example, although
interesting, is just a case-report, so results cannot prove causation and may not be generalizable.

Dyslexia
Dyslexia (DL) is a complex term characterized as a reading disorder. Subjects usually have normal
intelligence and features that differentiate it from language impairments in patients with mental
retardation [133] . Problems can include difficulty in spelling or writing words, reading quickly, pronouncing
words mentally or when reading aloud, and understanding what the individual is reading [134] . Some authors
consider dyslexia as an associated condition of developmental language disorder [135] or ADHD [136,137] . As
noted, the truth is that many patients exhibit alterations in speech and language. Silencing of some of the
most important genes involved in rodents, such as DCDC2, KIAA0319 and DYX1C1, produces deficits
in neuronal migration, dyslexia, and alterations in working memory, auditory processing and visual
attention [138] . Within the human genome, genetic mapping reports have identified regions of different
chromosomes, known as DYX loci [139-143] and other related genes.

Dyslexia susceptibility 1 candidate gene 1
In animal models, DYX1C1 (15q21) mutations generate a neuronal migration disorders that correlates with
DL. DYX1C1 knockdown in zebrafish results in alterations in the primary cilia, such as body curvature