The mechanisms underlying doxorubicin’s pharmacodynamics in cancer cells involve its conversion to an unstable metabolite, semiquinone, by enzymes such as NAD(P)H quinone dehydrogenase 1 (NQO1), nitric oxide synthases (NOS3), and xanthine oxidase (XDH), followed by reconversion to doxorubicin, releasing reactive oxygen species (ROS). This evidence concerns the gene NOS3 and cancer.