Since lower dopamine availability in the synaptic cleft might facilitate the antipsychotic blockade of DRD2 and thus influence the AIP risk, both the CYP2D6 variants that could influence the capacity of haloperidol metabolism, as well as the variants of the SLC6A3, HTR2C and HTR6 genes, that could modulate the dopamine release, might contribute to the potential of haloperidol-induced parkinsonism development. Here, HTR6 is linked to Parkinsonism.