In agreement with findings that translational regulation was broadly perturbed in various neurodegenerative diseases,19, 20, 21 and loss of proteostasis is an AD hallmark,22, 23 our in vivo ChaC-MS identification of G9a interactions with translation regulators such as METTL3 revealed a new, noncanonical function of G9a in the translational or post-translational regulation of AD pathogenesis. This evidence concerns the gene EHMT2 and Alzheimer disease.