hypothesis, we focused on genes that cluster within the M2c module and examined whether the distribution of the differentially expressed genes significance (estimated as −log10 P value) is different for genes with (“Drug”) and without (“NonDrug”) a drug signature. We did not find a significant difference in the distribution of −log10 P values for genes that have or do not have drug signature (drug versus non-drug: Kolmogorov–Smirnov test: P = 0.54). Therefore, our results do not support the hypothesis that drugs drive the loss of density through alteration in the transcript abundance of target genes. We also explored whether “Drug” versus “NonDrug” signatures within the M2c module show a different effect for loss or gain of connectivity in controls compared to SCZ. We did not observe any significant effect (Kolmogorov–Smirnov test: P = 0.054). This analysis provides additional evidence that the density loss in SCZ is not driven by medication effects.
