Considering the well-documented associations between m6A dysregulation and AD-related synaptic dysfunction, we propose that a deficiency in METTL16 may disrupt MAT2A-dependent SAM production, thereby impairing m6A homeostasis and exacerbating Aβ pathology, synaptic loss, and cognitive deficits characteristic of AD. This evidence concerns the gene METTL16 and Alzheimer disease.