A recent study by Mu et al. reported the rescue of cognitive deficits in an Alzheimer’s disease (AD) mouse model injected with Aβ1–42 aggregates via intraventricular administration of JNJ-63533054, as well as the amelioration of neuronal apoptosis and synaptotoxicity of medial septum cholinergic neurons in APP/PS1 transgenic mice via the overexpression of the GPR139 receptor [55]. The gene discussed is APP; the disease is Alzheimer disease.