In the CUMS model, MST1 activation impairs hippocampal synaptic plasticity and abnormally activates microglia, increasing neuroinflammation; while reducing MST1 levels reduces microglia activation, suppresses inflammatory responses, and promotes synaptic plasticity through the BDNF/AKT/CREB signaling pathway to counter depressive behavior and cognitive impairment caused by CUMS (Xu et al., 2021). The gene discussed is MST1; the disease is Cognitive impairment.