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. This evidence concerns the gene CYP2D6 and autoimmune pancreatitis.