In a model of Alzheimer’s disease, the SRG-mediated enhancement of the interaction between the inhibitor of apoptosis-stimulating protein of p53 (iASPP) and Keap1 upregulates Nrf2 activity and leads to increased synaptic plasticity and the rescue of cognitive impairment [83]. The gene discussed is KEAP1; the disease is early-onset autosomal dominant Alzheimer disease.