It is well documented that several neuropsychiatric disorders, including substance use disorders (SUDs), share symptoms, which could be the result of shared genetic underpinnings [1, 2]. Much of the heritability (h2) of genetically complex or polygenic brain disorders—e.g., schizophrenia (SCZ), Parkinson’s disease, and alcohol use disorder—is due to common genetic variation [3]. In addition, genome-wide association studies (GWASs) have deepened the understanding of such disorders, unraveling thousands of associated loci [4, 5]. However, elucidating disease mechanisms has remained challenging. One reason is missing heritability, meaning the gap between twin-based and single-nucleotide polymorphism (SNP)-based h2 estimates, which may result from limited statistical power, phenotypic heterogeneity, clinical misclassification, GWASs not probing associations with rare variants, epigenetics, genomic interactions, and structural genomic alterations [6]. Due to missing heritability, underlying causal genetic contributors might remain undetected. This impedes the translation of GWAS associations into their functional effects. Another reason explaining why elucidating disease mechanisms in neuropsychiatric disorders has remained challenging is that over 90% of identified variants are located within non-coding regions of the genome, indicating that regulatory elements—e.g., promoters, enhancers, and insulators—may explain
