Based on the aforementioned data, we hypothesized that MIA might modulate the CX3CL1–CX3CR1 and/or CD200–CD200R pathways, as well as microglia phenotypes in offspring rats subjected either to a prenatal challenge (MIA, as one hit) or to a “two-hit” model of schizophrenia (MIA combined with additional acute immune stimulation), which would lead to the occurrence of distinct behavioural phenotypes in adulthood. The gene discussed is CD200R1; the disease is schizophrenia.