## 6 Perspectives and Conclusions  
It is clear that altered iron metabolism occurs in cancer and leads to increased labile iron pools in the cytosol, mitochondria and lysosomes. The mitochondrial labile iron pool provides iron to essential Fe clusters involved in DNA replication and repair, which aids in sustained proliferation. Nonetheless, Fe-S clusters are more susceptible to ROS, which can impair the function of proteins with Fe-S clusters. Iron chelators have demonstrated that they can remove iron from the labile iron pool in the mitochondria and cytosol. This results in less iron being available for incorporation into Fe-S clusters for DNA replication and repair. The most obvious example is RnR inhibition, which is one mechanism by which chelators can inhibit tumour cells. More recently, iron chelators have been designed for various purposes. These purposes include: inhibiting topoisomerase, targeting specific DNA repair enzymes, and causing DNA breaks and apoptosis, to name a few [69; 161]. Iron chelators have also been designed to cause DNA damage by inducing ROS, which causes cell cycle arrest that inhibits cancer [176]. This expands the areas which need to be researched, such as, can iron chelators that produce ROS target Fe-S centres by inducing ROS whilst also limiting the labile iron pool? Thus, it would target the labile iron pool, i.e., the iron available for incorporation into these Fe-S clusters and the clusters themselves. Whether iron chelators can affect Fe-S clusters in necessary repair and replication enzymes, it is already clear that iron chelators are an attractive therapeutic option by limiting iron and reducing or increasing ROS. Iron chelators tackle altered iron metabolism in cancer by many different mechanisms in cancer cells, such as targeting proliferation, migration and invasion. The field of iron chelators started by addressing iron overload; thus, iron chelators were not explicitly designed for cancer. A crossover was noticed in that most iron chelators could inhibit RnR and therefore had therapeutic potential in cancer. More recently, iron chelators are starting to have more significant design considerations for those that can induce ROS either by inhibiting antioxidants or resulting in redox-active complexes culminating in DNA damage. Iron's role in cancer is deeply connected to many steps, with enhanced iron being a characteristic of most cancer cells due to the high demand for DNA replication. The increased amount of labile iron in cancer cells can result in ROS and genomic instability, ensuring an environment where tumour cells thrive via mutations and evolution. That being said, knowing iron's altered and crucial role in cancer, its essential role in DNA replication and repair through key enzymes and its role in causing genomic instability, there needs to be greater emphasis on creating iron chelators that can induce ROS for cancer, or that can target the mitochondria; specifically, the site of Fe-S biogenesis. The use of redox active iron chelators that could specifically target the mitochondria could increase the potency of these drugs for targeting cancer. Further research still needs to be completed in using iron chelators in combination therapy with synergistic compounds that can aid in ROS development. The following supporting information can be downloaded at: [[https://www.mdpi.com/article/10.3390/app121910161/s1](https://www.mdpi.com/article/10.3390/app121910161/s1)]([https://www.mdpi.com/article/10.3390/app121910161/s1](https://www.mdpi.com/article/10.3390/app121910161/s1)), Figure S1 shows redox active iron chelators mentioned in this paper their structure and iron binding groups. [PERSON] wrote this manuscript. [PERSON] and [PERSON] reviewed and edited this manuscript. All authors have read and agreed to the published version of the manuscript. This research received no external funding. Data Availability Statement: Not applicable. We would like to thank Biorender for the provision of their website for construction of our figures.