While the exact mechanism for the lower risk of parkinsonism among atypical APs is unknown, serotonin type 2A (5-HT2A) blockade, 5HT-2A: dopamine type 2 (D2) blockage ratio, and rate of association and dissociation at D2 receptors of atypical APs relative to typical APs are proposed explanations [16–20]. This evidence concerns the gene HTR2A and Parkinson disease.