Furthermore, given Abl1’s role in cancer, we hypothesize that modulating the Abl1/p53/p73 axis will be of therapeutic benefit not only in alleviating cardiac toxicity but also in regards to disease progression as shown in heavily pretreated gastrointestinal sarcoma tumor patients where low-dose combinations of Imatinib enhanced the anti-tumour activity of doxorubicin [201]. The gene discussed is TP53; the disease is neoplasm.