Our observations of the dependence of breast cancer cell survival on PRDX1 under the oxidative stress conditions, prompted us to combine PRDX1-targeting with the clinically applicable prooxidant agent, sodium L-ascorbate (L-ASC).26 When used in concentrations higher than physiological, L-ASC is known to generate excessive quantities of hydrogen peroxide.27 The gene discussed is PRDX1; the disease is breast cancer.