Postmortem studies also highlight reductions in cholinergic and GABA activity in the absence of major neuronal or synaptic loss, suggesting functional rather than structural changes may contribute to VH.37 In PD, increased 5HT2a binding has been linked to VH in postmortem38 and in vivo neurotransmitter binding studies.39 This may also help explain why the 5HT2a inverse agonist pimavanserin is effective treatment for hallucinations in PD. The gene discussed is HTR2A; the disease is Parkinson disease.