Epigenetically driven GAS2L3 enforces non-canonical cell cycle progression to promote osimertinib resistance in lung adenocarcinoma
These results uncover a metabolism-epigenetics–cell cycle interface that may represent a therapeutic vulnerability in EGFR-mutant LUAD and identify a glycolysis–H4K8la–GAS2L3 axis that drives noncanonical cell-cycle reprogramming independently of classical Cyclin–CDK activation, thereby promoting acquired osimertinib resistance.