development (e.g., neuronal growth, synaptic plasticity) [33]. FOXP2 was first identified two decades ago when rare heterozygous mutations of the gene were linked to a monogenic disorder involving speech motor deficits, accompanied by impairments in expressive and receptive language [34, 35]. Nevertheless, there is scant evidence that common FOXP2 variants contribute to inter-individual differences in language function [36, 37]. Though prior behavioral research [38-40] reported a link between language problems and ASB, it is premature to over-interpret the FOXP2 findings here. SNPs at this locus have been associated, through GWAS, with a range of externalizing traits, including ADHD [41], cannabis use disorder [42], and generalized risk tolerance [43]. Given the involvement of SNPS at this locus in different behavioral traits and diagnoses, and considering the small effect sizes, it is clear the association of FOXP2 variation with ASB has limited explanatory value on its own. That said, nothing yet precludes the possibility that this SNP may help to yield deeper insights once placed in broader context by future research.
