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Considering microenvironments in and around malignant tumours, the haem concentration in cancer cells is likely to be elevated through multiple mechanisms, such as (i) an increased intake of haem, (ii) mutation of enzymes in TCA cycle (for example, fumarate hydratase) that increases the level of succinyl CoA, a substrate for haem biosynthesis and (iii) metastasis to haem-rich organs such as liver, brain and bone marrow 46,47,48