In a mouse model of AD (expressing human Aβ), heterozygous deletion of beclin 1 (a protein that participates in the regulation of autophagy) resulted in a reduction of autophagy which, in turn, generated an exacerbated AD pathology, including extra- and intracellular Aβ deposition and neurodegeneration [91]. The gene discussed is BECN1; the disease is Alzheimer disease.