Dopaminergic dysfunction, including reduced dopamine transporter activity, has also been implicated in primary and secondary delusional parasitosis, providing a mechanistic rationale for antipsychotic therapy [10]. Demyelinating lesions may trigger neuropathic pruritus and subsequent somatic preoccupation, as illustrated in Figure 1, which outlines the proposed mechanism linking MS-related neuropathic pruritus to delusional parasitosis. The gene discussed is SLC6A3; the disease is parasitic infectious disease.