KEAP1 and ischemic stroke: Acetylation has been reported to mediate Nrf2 function in ischaemic stroke, and the histone deacetylase inhibitor trichostatin A (TSA) increases neuronal cell viability and reduces infarct volume, which is related to reduced expression of the Nrf2 suppressor Keap1, increased Keap1/Nrf2 dissociation and Nrf2 nuclear translocation [60].