Studies of an AD mouse model (APP/PS1 transgenic mice) have revealed that the mice display increased m6A methylation in the cortex and hippocampus, and that expression of Mettl3 is increased whereas Fto expression is reduced in the AD mice [62, 63]. These studies support that dysregulation of the Mettl3/Fto axis may alter global patterns of m6A methylation of mRNAs, further impacting dendritic development, synaptic growth, synaptic assembly, axon guidance, and long-term potentiation, thereby potentially linking m6A epitranscriptomic regulation and neurological disorders. The gene discussed is METTL3; the disease is Alzheimer disease.