To dissect a G9a-mediated mechanism of AD pathogenesis and the corresponding action mechanism of MS1262 reversal of AD symptoms, we performed ChaC-MS and tandem mass tag (TMT)-based quantitative proteomics/phosphoproteomics experiments 27, 29 using microdissected hippocampal samples from the same mouse cohorts used for the aforementioned behavioral studies (Fig. 3 and Fig. 4). This evidence concerns the gene EHMT2 and Alzheimer disease.