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We therefore propose a simple, testable framework: CSCs from embryonal/embryonic-like tumors may depend on ferritin chiefly to buffer iron and preserve stemness under fluctuating microenvironments, whereas CSCs from differentiated epithelial tumors may exploit iron in specialized metabolic or redox processes, In this context, ferritin loss can trigger stress-adaptive programs (proliferation, migration, EMT) that paradoxically increase aggressiveness [123,124,125]

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Moreover, STS was successfully administered to treat toxic overdoses of cisplatin, a chemotherapy drug, in the clinical setting [10]