Considering all these observations in the human brain and in mouse models of the disease, authors suggested that having two copies of Kdm6a compared to just one copy of the gene confers stronger resilience to the disease, and speculated that increased KDM6A in brains of people with Alzheimer’s disease might be a neuroprotective, compensatory response [43]. Here, KDM6A is linked to early-onset autosomal dominant Alzheimer disease.