(57) found that Mettl3 deletion in monocyte-derived macrophages (Mettl3fl/flLyz2Cre/-) reduces the m6A modification on DNA methyltransferase 3A (Dnmt3a) mRNA and impairs YTHDF1-mediated Dnmt3a translation, which in turn interacts with alpha-tubulin acetyltransferase 1 (Atat1) promoter to maintain its expression, improving cognitive function in an amyloid beta (Aβ)-induced Alzheimer’s disease (AD) mouse model. Here, YTHDF1 is linked to Alzheimer disease.