The considerable enhancement in hippocampal synaptic plasticity and dendritic spine density by FGF21 [54], along with its protective effects against Alzheimer’s disease (AD)-like pathologies induced by Aβ25-35 peptide [55] and cognitive impairment induced by D-galactose and an HFD [56], led us to hypothesize that the GLN-induced increase in FGF21 may significantly contribute to the enhanced learning and memory functions in mice (Figure 1). The gene discussed is FGF21; the disease is early-onset autosomal dominant Alzheimer disease.