Autism Spectrum Disorders (ASD) are neurodevelopmental conditions that are highly heritable but also genetically very heterogeneous. Current genetic data estimates that over 1000 loci contribute to the genetic landscape of ASD. To identify molecular pathways dysregulated downstream these heterogeneous genetic variants, we and others have utilized co-expression networks to interrogate transcriptome changes in ASD brain and to further integrate transcriptome data with genetic association data. Despite the genetic heterogeneity of ASD, a replicable molecular signature of ASD brain has been identified by several studies using distinct cohorts (Voineagu et al. Nature 2011, Liu et al. Plos Genetics 2016, Parikshak et al. Nature 2016). One of the genes consistently dysregulated in the brain of ASD patients is the neuronal and muscle specific splicing factor RBFOX1. Several lines of evidence indicate that in addition to its role in splicing regulation, RBFOX1 has an effect on transcript abundance. Here we investigate the hypothesis that RBFOX1 might affect transcript abundance by regulating the formation of circular RNA molecules. Circular RNAs (circRNAs) result from non-canonical back-splicing, and have been shown to regulate the expression of their parental genes by acting as miRNA sponges and binding to RNA Pol II at the promoter. To investigate the effect of RBFOX1 on circRNA biogenesis, we stably overexpressed the neuronal isoform of RBFOX1 in human primary astrocytes, where RBFOX1 is not endogenously expressed. We carried out RNA-seq on triplicate RBFOX1 overexpression and control samples, with and without RNaseR treatment, to enrich for circular RNA molecules. We observed a strong increase in circRNA expression in cells stably expressing RBFOX1. We identified 85 robustly expressed circRNAs in control primary astrocytes, and over 500 circRNAs in cells stably expressing RBFOX1. circRNA detection was strongly enhanced by RNaseR treatment, as expected. We validated the circular nature of a subset of RBFOX1-induced circRNAs by RT-PCR/Sanger sequencing, with 90% validation rate. The parental genes of RBFOX1-dependent circRNAs previously shown to associate with RNA Pol II (Li et al. Nat.Struct.Mol.Biol. 2015) showed increased expression levels in RBFOX1-expressing cells. We also found a significant overlap between RBFOX1-dependent circRNAs and circRNAs previously shown (Zhang et al. Cell.Rep. 2016) to be induced upon neuronal differentiation. These data bring initial evidence for the role of RBFOX1 in regulating the formation of circRNAs in the human brain, a mechanism potentially contributing to its role in ASD.