In line with the reported clinical benefit of trazodone in Parkinson disease patients [56], our model suggests that cortical 5-HT2A activity is a key modulator of EPS liability and that the fast dissociation rate of JNJ37822681 may only compensate partially for the EPS liability induced by significant D2 receptor inhibition during burst firing, This is not unlike remoxipride that has a substantial EPS liability despite a low affinity for the D2 receptor [57]. The gene discussed is HTR2A; the disease is Parkinson disease.