As a vital mediator of cell death in response to cell cycle arrest, apoptosis, cell survival, and genomic stability, GADD45b is implicated in the pathogenesis of multiple neurological diseases.[45, 46, 47] In line with this, we here found that GADD45b knockdown reversed MK801‐induced cognitive impairments whereas overexpression of GADD45b in wild‐type rats resulted in severe neuronal loss and synaptic dysfunction in the hippocampal CA1 region and caused cognitive deficits. The gene discussed is GADD45B; the disease is nervous system disorder.