These observations suggest two different concepts: 1) that transition-metal based CORMs can decrease the expression of HO-1 in TNBC, a mechanism not followed by the non-transition metal-based CORM-A1, and 2) that this downregulation might lead to a higher sensitivity of these cells towards other chemotherapeutic or anti-angiogenic agents, based on previous observations for other tumour types [70]. This evidence concerns the gene HMOX1 and neoplasm.