Charting the regulatory interactions between transcription factors (TFs), enhancers, and genes during the formation of neuronal lineages in human can help decipher the complex genetic etiologies of neurodevelopmental disorders such as autism spectrum disorder (ASD). To achieve this, we conducted an integrative analysis of epigenomic and transcriptomic profiles of human forebrain organoids derived from individuals with idiopathic ASD and their neurotypical fathers. This multi-omics profiling allowed us to build an enhancer-driven gene regulatory network of early neural development and relate its activity to changes in cellular composition found in organoids from ASD individuals. We observed that excitatory neurogenesis was more exuberant in ASD individuals with macrocephaly and on the contrary repressed in other ASD cases. The regulatory network linked transcriptomic signatures of ASD to altered activity of key TFs such as BHLHE22, FOXG1, EOMES, and NEUROD2, which are major drivers behind changes in excitatory neuron production. These imbalances suggest that ASD could results from altered regulatory program specifying neuronal cell lineages in the fetal forebrain. Thus, modeling individuals’ early brain development in organoids provides insights into the etiology of idiopathic ASD and can guide future experimental approaches to decipher its genetic heterogeneity.