Fig. 2
Multiomics analyses. Genetic and epigenetic factors reflecting treatment response were investigated by meQTL and DMR, and the results were refined using three different approaches. a Upon comparison of meQTLs, risk-DMRs, and RES-DMRs, 324 genes were identified as ASM genes associated with SCZ risk and treatment response. b Within the ASM genes, colocalization identified four signals, including rs11125746 in LINC01795, rs12674515 in DDHD2, rs28759130 in SBNO1, and rs498541 in KCNG2. c PAI identified 14 genes showing significant differences in overall PAI strength under the case‒control condition and non-RES versus RES condition. Among them, RUFY1 displayed brain‒blood consistency in methylation, transcription, and chromatin interaction, along with a significant difference in PAI strength. d EWAS identified one genome-wide significant (Padj < 1 × 10–8) signal located in the SEMA7A gene. Solid and dashed gray lines represent genome-wide and suggestive significance, respectively. meQTL. Methylation quantitative trait loci; DMR. Differentially methylated region; PAI. Promoter-anchored chromatin interaction; SCZ. Schizophrenia; RES. Response; ASM. Allele-specific methylated; GWAS. Genome-wide association study; PP4. Posterior probability for a shared signal; SMR. Summary-based Mendelian randomization; LINC01795. Long intergenic non-protein coding RNA 1795; DDHD2. DDHD domain containing 2; SBNO1. Strawberry notch homolog 1; KCNG2. Potassium voltage-gated channel modifier subfamily G member 2; RUFY1. RUN and FYVE domain containing 1; MIR885. microRNA 885, BEGAIN brain enriched guanylate kinase associated; SLC7A7. Solute carrier family 7 member 7; KLF5. KLF transcription factor 5; SEMA7A. Semaphorin 7A