Several factors seem to be implicated in the vulnerability of EC in AD, including the dysregulation of brain-derived neurotrophic factor and the ARMS/Kidins220 scaffold protein; the activation of stress-related kinases and neuroinflammatory processes; and the downregulation of neurotransmitter receptors, including N-methyl-D-aspartate (NMDA) subtype 1 glutamate receptor, muscarinic acetylcholine receptor 1, and γ-Aminobutyric acid type A (GABAA) receptor delta (reviewed in the work of [13]). The gene discussed is CHRM1; the disease is Alzheimer disease.