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Shillington A, Pedapati E, Hopkin R, Suhrie K. Early behavioral and developmental interventions in ADNP‐syndrome: A case report of SWI/SNF‐related neurodevelopmental syndrome. Mol Genet Genomic Med. 2020;8:e1230 10.1002/mgg3.1230 1. BACKGROUND {#mgg31230-sec-0005} ============= Autism Spectrum Disorder (ASD) is a developmental disorder characterized by impairments in social communication, along with restrictive interests and repetitive behaviors that are typically present by 2 years of age. ASD currently affects approximately one in 59 children, and the incidence has been on the rise (Wingate et al., [2014](#mgg31230-bib-0020){ref-type="ref"}). Both genetic and environmental factors are thought to be causative in the etiology of ASD which lead to changes in neuronal development, growth of the brain, and synaptic connectivity. As next‐generation sequencing (NGS) becomes more available and more affordable, many families along with their physicians are electing to pursue NGS testing to elucidate a specific molecular diagnosis for patients with ASD. It is reported that more than 2,000 genes are involved in ASD, and that no one gene is likely to explain more than 1% of cases (De Rubeis et al., [2014](#mgg31230-bib-0005){ref-type="ref"}). The rarity of any one genetic mechanism of disease can make it very difficult to develop interventions and care plans for patients when there may be only a handful of patients reported to have the same genetic change. One gene that is commonly sequenced as part of NGS evaluation is the activity‐dependent neuroprotector homeobox (*ADNP*) gene, and may be one of the most common single‐gene causes of ASD; mutations in this gene are thought to explain the etiology of 0.17% of patients with ASD (Helsmoortel et al., [2014](#mgg31230-bib-0009){ref-type="ref"}). The *ADNP* protein product is thought to be a regulator of axonal transport and dendritic spine plasticity at the synapse level (Gozes, Patterson, et al., [2017](#mgg31230-bib-0006){ref-type="ref"}; Gozes, Patterson, et al., [2017](#mgg31230-bib-0006){ref-type="ref"}), specifically functioning as a regulator of the essential chromatin‐remodeling complex, SWItch/sucrose non‐fermentable (SWI/SNF; Mandel & Gozes, [2007](#mgg31230-bib-0013){ref-type="ref"}; Figure [1](#mgg31230-fig-0001){ref-type="fig"}). ![The SWI/SNF chromatin remodeling complex *Source*: Mandel et al (2007)](MGG3-8-e1230-g001){#mgg31230-fig-0001} The connection between ADNP and the SWI/SNF complex is clinically relevant, as genetic disorders within this family of genes are well described and have neurodevelopmental feature overlap. The C‐terminal of ADNP directly interacts with ARID1A*,* SMARCA4, and SMARCC2, three essential components of the SWI/SNF complex. ADNP appears to be a regulator of SWI/SNF function, thus ultimately impacting chromatin remodeling which is essential for postmitotic activity‐dependent dendritic outgrowth and axonal development. Mutant ADNP protein appears to compete with wild‐type protein preventing optimal SWI/SNF complex function (Helsmoortel et al., [2014](#mgg31230-bib-0009){ref-type="ref"}). Deficiencies in a working SWI/SNF complex lead to defects in neuronal development (Lessard et al., [2007](#mgg31230-bib-0012){ref-type="ref"}). Most patients diagnosed with ADNP Syndrome, also known as Helsmoortel--Van Der Aa Syndrome, have ASD as a comorbidity, and all patients have mild‐to‐severe intellectual disability (Arnett et al., [2018](#mgg31230-bib-0002){ref-type="ref"}; Helsmoortel et al., [2014](#mgg31230-bib-0009){ref-type="ref"}; Van Dijck et al., [2019](#mgg31230-bib-0019){ref-type="ref"}). Other frequent findings include hypotonia, delayed developmental milestones including prominent speech delays of little to no words to some simple sentences, feeding problems in infancy followed by GI problems such as gastroesophageal reflux disease (GERD) and