Remarkably, this study showed that a lentivirus-driven HDAC1::SUMO translational fusion protein could rescue the learning and memory deficits of an APP/Presenilin 1 murine model of Alzheimer's disease (Tao et al., 2017), suggesting that HDAC1 SUMOylation may be neuroprotective in response to Aβ accumulation. This evidence concerns the gene HDAC1 and early-onset autosomal dominant Alzheimer disease.