Our data supports recent findings implicating histaminergic neurotransmission in the etiology or modulation of tics and highlights the potential involvement of GABAergic mechanisms as well. In addition, the results reinforce the notion of shared genetic risks among clinically-distinct syndromes, in this case ASD and tic disorders, and identify three novel, large, rare, genic, de novo CNVs that are likely carrying risk in the individuals in which they were identified, based on their de novo status and high gene content relative to controls.
