Thus, we tested Abca7 null mice in behavioural tasks relevant to schizophrenia: Abca7 deficient mice showed unaltered baseline locomotion and sensorimotor gating but female Abca7−/− appeared to have longer-lasting susceptibility to the locomotion-stimulating effects of acute MK-801 treatment, which might indicate changes to the glutamatergic system, the processing of MK-801, or more specifically the NMDA receptor sensitivity/expression levels. Here, ABCA7 is linked to schizophrenia.