Remarkably, several points of evidence suggest this cryptic paracentric inversion as at least equally likely to explain the patient’s phenotype than disruption of any of the NDD candidate genes within the cytogenetically visible BCAs: A recent study in a large cohort of individuals with NDD and autism spectrum disorders [5] identified two symptomatic carriers, father and son, of a reciprocal translocation that truncated ZNF804A 229 kb downstream of the end of its 3′-untranslated region. This evidence concerns the gene ZNF804A and Neurodevelopmental delay.