In accordance wefind that the dual insult of oxidative damage caused by Bmi-1 knockdown andcisplatin treatment, which is known to cause double strand breaks in the DNA alongwith ROS production tips the threshold for ovarian cancer cells towards apoptosis byinducing phosphorylation of i) Chk2 and H2AX, ii) causing nuclear foci formation by53BP1 and cleavage of apoptotic markers such as iii) caspases and PARP. The gene discussed is BMI1; the disease is ovarian carcinoma.