Instead, in the early-onset/familial AD cases the mutated gene responsible for the Aβ overproduction is the uncontested primum movens. Yet, even in this hereditary AD form the CaSR interaction with the overproduced Aβs is likely to significantly aggravate the brain amyloid burden by further intensifying the overproduction of Aβs and of all the other noxious agents its signaling induces, thus detrimentally accelerating the clinical course. The gene discussed is DDX41; the disease is Alzheimer disease.