This study investigates the transcriptomic differences between autistic and normal brains using gene co-expression network analysis. The researchers found significant differences in gene expression patterns, particularly in the frontal and temporal cortices, suggesting abnormalities in cortical patterning. They identified two main modules of co-expressed genes: a neuronal module enriched for autism susceptibility genes, including A2BP1/FOX1, and an immune-glial module enriched for immune genes and glial markers. High-throughput RNA sequencing revealed dysregulated splicing of A2BP1-dependent alternative exons in ASD brains. Additionally, the neuronal module showed enrichment for genetically associated variants, while the immune-glial module did not, indicating a non-genetic etiology for this process. These findings provide strong evidence for convergent molecular abnormalities in ASD and implicate transcriptional and splicing dysregulation as underlying mechanisms of neuronal dysfunction.This study investigates the transcriptomic differences between autistic and normal brains using gene co-expression network analysis. The researchers found significant differences in gene expression patterns, particularly in the frontal and temporal cortices, suggesting abnormalities in cortical patterning. They identified two main modules of co-expressed genes: a neuronal module enriched for autism susceptibility genes, including A2BP1/FOX1, and an immune-glial module enriched for immune genes and glial markers. High-throughput RNA sequencing revealed dysregulated splicing of A2BP1-dependent alternative exons in ASD brains. Additionally, the neuronal module showed enrichment for genetically associated variants, while the immune-glial module did not, indicating a non-genetic etiology for this process. These findings provide strong evidence for convergent molecular abnormalities in ASD and implicate transcriptional and splicing dysregulation as underlying mechanisms of neuronal dysfunction.