While our results provide initial evidence

While our results provide initial evidence for the association between 5-HTTLPR genotypes and individual differences in selective attention in typically developing children, certain limitations of our study require consideration. First, the participants in this study were recruited from lower SES families, as discussed above. While some studies reported stronger genetic influences in lower SES populations (Nobile et al., 2007, 2010; Williams et al., 2008), others associated weaker genetic influences with lower SES (Schwartz, 2015; Tucker-Drob et al., 2011; Turkheimer et al., 2003). Further, a recent meta-analysis argued for large cross-national differences in gene-by-SES interactions (Tucker-Drob and Bates, 2015). Given a lower SES environment is itself a risk factor for poorer neural mechanisms of attention (D\'Angiulli et al., 2008; Stevens et al., 2009), it remains to be investigated whether the effects of 5-HTTLPR and socioeconomic status are additive or interactive. Second, based on parent reports, our participants were predominantly of Caucasian ancestry. This raises the question as to whether our findings would generalize beyond a sample of Caucasian ancestry. It has been demonstrated that the frequency and functional characteristics of 5-HTTLPR may differ across populations (Chiao and Blizinsky, 2010; Odgerel et al., 2013; van Ijzendoorn et al., 2012). For instance, being hdac inhibitors for the short allele was associated with lower serotonin function in the central nervous system in European-Americans, and higher serotonin function in African-Americans (Williams et al., 2003). As another example, differential susceptibility of the short allele to environmental factors was observed in samples composed of primarily White children (van Ijzendoorn et al., 2012), while in a sample of predominantly Black children, homozygous long allele carriers were found to show greater susceptibility to environmental effects (Davies and Cicchetti, 2014). Therefore, the extent to which our findings would generalize to more diverse populations of lower SES children remains to be investigated. Another limitation of our study is the biallelic categorization of the 5-HTTLPR allelic variations. Here we focused on the two common allelic variants that occur either as a shorter sequence of 14 repeats (short allele) or a longer sequence of 16 repeats (long allele). However, other lengths have also been reported (Kraft et al., 2005; Nakamura et al., 2000). Furthermore, instead of a biallelic categorization, a triallelic classification has been proposed based on the single nucleotide variant (A to G) detected on the long allele (Hu et al., 2006; Kraft et al., 2005). The variant designated LA was associated with higher serotonin transporter binding, whereas the variant designated LG was associated with lower serotonin binding (Hu et al., 2006; Praschak-Rieder et al., 2007). According to this categorization, the LG variant is grouped together with the short allele, in comparison to the LA/LA genotype assigned to long homozygosity (Davies and Cicchetti, 2014; Enge et al., 2014; Mileva-Seitz et al., 2011). If we had used this triallelic categorization, children who carry the LG variant would be grouped together with short carriers, instead of long homozygotes. It will be important to test this triallelic variation approach in future studies of 5-HTTLPR genotype and brain functioning. In addition, it bears repeating that as no single candidate gene can solely account for variability in any cognitive ability, thus it remains crucial to investigate how 5-HTTLPR polymorphism interacts with other polymorphisms linked to attentional abilities in children. In adults, single nucleotide polymorphisms (SNPs) of various genes have been linked to cognitive abilities (Green et al., 2008; Savitz et al., 2006). Among these, polymorphisms of several genes have been associated with attentional abilities (Stormer et al., 2012). These genes include, but are not limited to, catecholamine-O-methyltransferase (COMT) gene, cholinergic receptor, nicotinic alpha 4 (CHRNA4) gene, dopamine receptor D4 (DRD4) gene, and dopamine active transporter 1 gene (DAT1). In typically developing infants and children, variability in attentional abilities has also been linked to COMT and DAT1 polymorphisms (Holmboe et al., 2010; Markant et al., 2014; Rueda et al., 2005). A more comprehensive array of candidate genes, and assessment of their interactions with each other, would greatly advance our understanding of biological foundations of individual differences in neural mechanisms of selective attention.