relevance to SCZ risk, we tested if the co-expression pattern for M2c was perturbed in SCZ samples relative to controls. We used two categories of network-based preservation statistics: (a) testing whether highly connected nodes in a module remain as highly connected (“density”), or (b) testing for differences in the overall connectivity pattern in a module (“connectivity”). The M2c module exhibits a loss of density in the SCZ cases (permutation Z = −1.79, one-tailed P = 0.037, Fig. 6B) but no loss of connectivity. The loss of density replicates in the HBCC cohort (Z = −3.02, P = 0.003), indicating that the regulatory coordination of genes in this module is disrupted in SCZ. The dysregulation of M2c in SCZ is not due to medication effect or clinical and technical confounds.
