We modeled DNAm levels as a function of diagnosis, and adjusted for age, race, and the first four PCs of the negative control probes on the microarrays (see Methods). These negative control PCs were strongly associated with processing plate and microarray slide (Supplementary Figure 10) – only the 4th negative control PC was marginally associated with diagnosis (p=0.003). After initial differential methylation analyses using all 431 samples, we noticed that one of the three processing plates containing both patients with schizophrenia and controls drove much of the differential methylation signal (Supplementary Figure 11), and therefore removed the samples from this plate and reran the analysis on 244 subjects (108 patients with schizophrenia and 136 controls), identifying 2,104 probes/CpGs significant at a Bonferroni-adjusted p < 0.05 (Supplementary Table 10). Almost all of these involved hypomethylation of individual CpGs in patients compared to controls (N=2,043, 97. 1%) with much smaller differences in methylation levels than those that found in the prenatal/postnatal contrast analysis (mean absolute proportion change: 0.013, IQR: 0.010–0.01.8). This pattern of diagnosis (i.e. state) associated hypomethylated CpGs contrasts with the
