Although at the selected concentrations (1 μM) they do not affect cell number or PARP cleavage, D and D4S completely prevent E2 effects, allowing the Pacl-induced activation of a pro-apoptotic cascade, even in the presence of the hormone, sustaining that the anti-estrogenic activity is pivotal for rendering cancer cells more vulnerable to the chemotherapeutic drug. The gene discussed is PARP1; the disease is cancer.