Reportedly, MLK3 activity is positively regulated by both autophosphorylation and upstream kinase-mediated phosphorylation at threonine 277 and serine 281 residues within the kinase domain [4], which plays an important role in cell death, contributing to the pathogenesis of ischemic brain damage, Alzheimer’s disease, and oxidative stress injury [10, 37, 48–50]. This evidence concerns the gene MAP3K11 and early-onset autosomal dominant Alzheimer disease.