Enhancing GBP2 activity in breast cancer, possibly via Drp-1 agonists, autophagy inducers, or small molecule activators targeting its GTPase domain, could suppress mitochondrial replication and tumor growth, capitalizing on its protective effects against metastasis—a strategy assessable through mitochondrial function assays, tumor size monitoring, or drug sensitivity screens [36,38]. Here, DNM1L is linked to neoplasm.