with gene expression functionality and that predicted an OCD hoarding subphenotype in our sample (Figure 1 and Figure 2). The possibility of 2 or more functional (possibly causal) variants of differential effect size provides 1 plausible explanation for the molecular discrepancies between present and published SLC1A1 genotyping studies in OCD, especially if these were found to be interacting from within different haplotype blocks. This possibility might be addressed by genotyping markers at higher density or by resequencing large genomic regions.
