Furthermore, the deletion of miR-301a led to the emergence of anxiety, cognitive, and social deficits, which are considered autism-like behaviors in mice, while the exogenous administration of a miR-301a inhibitor reduced maternal immune activation (MIA)-induced autism-like behaviors probably through the upregulation of SOCS3, which inhibits the release of proinflammatory cytokines [59]. The gene discussed is SOCS3; the disease is autism.