any of these scenarios, within the limits of statistical power, whereas regional analysis would likely detect DEG only for (1) or (2). If (3) would be a better model for most DE genes, global analysis has better power. Our small sample size has precluded our ability to rule out the contributions of several important covariates that may affect gene expression and the potential effect of diagnosis. These include potential effects of pharmacotherapy, substance use, and additional neurological and psychiatric diagnoses. It is worth noting that in a previous study of these same subjects, no impact of major depressive disorder (MDD) diagnosis or antidepressant, benzodiazepine, or tobacco use was observed on expression of synaptic transcripts in the OFC and striatum36. Third, although these data are broadly consistent with our previous report of downregulation of a small targeted set of glutamatergic transcripts assessed via qPCR across OFC and striatal brain regions in these same OCD subjects36, here we did not observe significant DEG in the OFC alone. Notably, on a gene-by-gene basis, the normalized qPCR expression from36 and the RNAseq gene expression levels reported here were significantly positively correlated as expected (r = 0.340, p < 0.0001, Table S11). It is therefore
