The therapeutic index is high when molecular targets overexpressed specifically in tumor cells can be targeted by small molecule inhibitors. Multi-kinase inhibitors have dramatically improved patient survival in hematologic malignancies, while drugs targeting cancer specific mutations have improved survival in select patient populations. In the mid-1970s, 5 year survival estimates were at 41% for patients diagnosed with acute lymphocytic leukemia while they are reported at 71% for patients diagnosed between 2006 and 2012. Similar improvement has been witnessed for chronic myeloid leukemia, 22% to 66% in the same time intervals . However, currently available standard chemotherapeutic agents and even the latest technologies in radiation physics fail to qualify as curative options for several cancer types. Commonly used chemotherapy regimens include platinum based DNA alkylating agents, topoisomerase poisons, antimetabolites, microtubule inhibitors, antitumor antibiotics, proteasome inhibitors etc. . Antitumor antibiotics include a class of drugs called anthracyclines that inhibit pathways that generate DNA nucleotides. Non anthracycline drugs in this class include a compound called bleomycin. Bleomycin portrays the strongest evidence for clustered DNA damage being used as the mechanism of action for a chemotherapeutic agent. The mechanism of action of bleomycin and the similarities in base damage produced when compared with IR makes it a “radiomimetic” chemotherapeutic . The drug creates reactive aldehyde groups at the sugar moiety that is capable of reacting with cytosine residues in its proximity and creating clustered DNA damage. Use of bleomycin has been inhibited due to severe pulmonary toxicity  and risk of pulmonary fibrosis despite tolerable myelotoxicity. Since the clinical trials establishing the correlation between bleomycin use and pulmonary toxicity in the 1980s  there has been years of research that indicates the importance of ROS at the site of action in propagation of the oxidative DNA damage. Even low levels of ROS have been reported to cause GI via NHEJ-mediated DNA repair .