An ASD "comorbidity" can have several fundamentally-distinct causal origins: it can arise due to shared genetic risk between ASD and non-ASD phenotypes (e.g., ASD and microcephaly in the context of the MECP2 mutation), as a "secondary symptom" of ASD when engendered by the same causal influence (e.g., epilepsy in channelopathies associated with ASD), due to chance co-occurrence of ASD with a causally-independent liability (e.g., ASD and diabetes), or as the late manifestation of an independent causal influence on ASD (eg, attention-deficit/hyperactivity disorder).
One patient's symptoms suggest an extension of the known spectrum of MECP2 associated phenotypes to include global developmental delay with obsessive compulsive disorder and attention deficit hyperactivity disorder.
Also, these findings add significant weight to the mounting evidence suggesting that the MeCP2_e1 isoform is the etiologically relevant form of the protein.