Genome-wide association studies (GWAS) have identified more than 100 loci that show robust association withschizophrenia risk. However, due to the complexity of linkage disequilibrium and gene regulatory, it is challenging topinpoint the causal genes at the risk loci and translate the genetic findings from GWAS into disease mechanism andclinical treatment. Here we systematically predicted the plausible candidate causal genes for schizophrenia atgenome-wide level. We utilized different approaches and strategies to predict causal genes for schizophrenia,including Sherlock, SMR, DAPPLE, Prix Fixe, NetWAS, and DEPICT. By integrating the results from different predictionapproaches, we identified six top candidates that represent promising causal genes for schizophrenia, includingCNTN4, GATAD2A, GPM6A, MMP16, PSMA4, and TCF4. Besides, we also identified 35 additional high-confidence causalgenes for schizophrenia. The identified causal genes showed distinct spatio-temporal expression patterns indeveloping and adult human brain. Cell-type-specific expression analysis indicated that the expression level of thepredicted causal genes was significantly higher in neurons compared with oligodendrocytes and microglia (P <0.05).We found that synaptic transmission-related genes were significantly enriched among the identified causal genes (P<0.05), providing further support for the dysregulation of synaptic transmission in schizophrenia. Finally, we showedthat the top six causal genes are dysregulated in schizophrenia cases compared with controls and knockdown of thesegenes impaired the proliferation of neuronal cells. Our study depicts the landscape of plausible schizophrenia causalgenes for the first time. Further genetic and functional validation of these genes will provide mechanistic insights intoschizophrenia pathogenesis and may facilitate to provide potential targets for future therapeutics and diagnostics.