The study investigates the role of mitochondrial dynamics in controlling T cell metabolism and fate. Activated effector T (T_E) cells exhibit aerobic glycolysis, while memory T (T_M) cells engage fatty acid oxidation (FAO). The research shows that T_E cells have punctate mitochondria, whereas T_M cells maintain fused networks. The fusion protein Opa1 is essential for T_M cell generation but not T_E cells. Enforcing fusion in T_E cells imparts T_M cell characteristics, enhancing antitumor function. Mitochondrial fusion in T_M cells configures electron transport chain (ETC) complex associations, favoring oxidative phosphorylation (OXPHOS) and FAO. In contrast, mitochondrial fission in T_E cells leads to cristae expansion, reducing ETC efficiency and promoting aerobic glycolysis. The study suggests that mitochondrial remodeling is a signaling mechanism that instructs T cell metabolic programming, with Opa1 playing a critical role in maintaining efficient ETC activity and redox balance in T_M cells.The study investigates the role of mitochondrial dynamics in controlling T cell metabolism and fate. Activated effector T (T_E) cells exhibit aerobic glycolysis, while memory T (T_M) cells engage fatty acid oxidation (FAO). The research shows that T_E cells have punctate mitochondria, whereas T_M cells maintain fused networks. The fusion protein Opa1 is essential for T_M cell generation but not T_E cells. Enforcing fusion in T_E cells imparts T_M cell characteristics, enhancing antitumor function. Mitochondrial fusion in T_M cells configures electron transport chain (ETC) complex associations, favoring oxidative phosphorylation (OXPHOS) and FAO. In contrast, mitochondrial fission in T_E cells leads to cristae expansion, reducing ETC efficiency and promoting aerobic glycolysis. The study suggests that mitochondrial remodeling is a signaling mechanism that instructs T cell metabolic programming, with Opa1 playing a critical role in maintaining efficient ETC activity and redox balance in T_M cells.