STING1 and neoplasm: The HBMn-FA nanoplatform drives ferroptosis in tumor cells, generating high levels of ROS that induce mitochondrial stress and release endogenous mtDNA, which synergizes with Mn2+ to activate the cGAS -STING pathway, while tumor-derived cytosolic dsDNA from ferroptotic cell debris further amplifies STING signaling in DCs and other antigen-presenting cells [146].