MIAT silencing enhanced breast cancer cell response to a diverse range of apoptotic stimuli acting via different mechanisms, including DNA damage (UV-C irradiation), inhibition of mouse double minutes clone 2 (MDM2) (nutlin-3a), microtubule stabilizing (docetaxel), inhibition of topoisomerase II (mitoxantrone), and inhibition of thymidylate synthase (5-fluorouracil), indicating that MIAT participates in a late common step that can connect the different apoptotic pathways activated by these agents. This evidence concerns the gene TYMS and breast cancer.