Moreover, a reduction in the levels of Mirta22 (an inhibitor of neuronal maturation whose expression is up-regulated in the brain of Df(16)A+/− mice as a result of the hemizygosity of DGCR8) [88] rescued not only key schizophrenia-related cognitive and behavioural dysfunctions, but also abnormalities in PFC synaptic and structural plasticity. The gene discussed is DGCR8; the disease is schizophrenia.