In MCAO mouse model of stroke, the expression of PIRB and its MHC-I ligands (H2-K and H2-D), go up and peak at around 7-day post-reperfusion [44,91]; the elevation in all three proteins appears to be neuronal [91], suggesting that previously described role for MHC-I and PIRB in promoting LTD [12,16,33,52] can contribute to the pathological synapse loss in the ischemic penumbra around the infarct zone. The gene discussed is LILRB1; the disease is stroke disorder.