This multi-hit hypothesis likely applies to the DMD condition, in which a full autistic-like phenotype would only be achieved in some patients when the mutation in the dmd gene alters expression of additional C-terminal dystrophin products [73] and/or when additional mutations or copy number variations (CNVs) in other genes disturb expression of other synaptic proteins, leading to cumulative deficits that would then meet criteria for ASD diagnosis [14, 74, 75]. This evidence concerns the gene DMD and Duchenne muscular dystrophy.