Notably, optogenetic activation or restoring Igfbp2 expression in glutamatergic projections from the PVT to the central amygdala (CeA) blocked anesthesia‐induced memory impairment, whereas optogenetic inhibition or knocking down of Igfbp2 expression in these projections is sufficient to engender similar memory impairment in control mice. The gene discussed is IGFBP2; the disease is memory impairment.