Phospholipids are the major component of cell membranes that compartmentalize metabolism and a variety of other processes. Not surprisingly, the regulation of the synthesis of phospholipids necessitates coordination with metabolic status. However, how cells might utilize membrane lipids in cellular and metabolic homeostasis is poorly understood. Among thousands of metabolic reactions, the transmethylation reaction is one of the most important and universal. The reaction transfers a methyl group from the donor S-adenosylmethionine (SAM) to a variety of cellular substrates, including proteins, lipids, nucleic acids, and cellular metabolites. These SAM-dependent methyltransferases engage in nearly every aspect of biology, thereby underscoring the importance of SAM homeostasis. I recently found in the yeast Saccharomyces cerevisiae that the methylation of particular phospholipid species is the major cellular consumer of SAM, and dysregulation of phospholipid methylation has remarkable consequences on other methylation events ongoing in the nucleus. Using a combination of approaches in genetics, metabolomics, and biochemistry, I addressed an underappreciated link between phospholipid metabolism and the maintenance of the epigenome. I propose a cellular strategy through which cells integrate epigenetic regulation with metabolic information from membrane lipids.