Similarly to what was reported for recently synthesized dual HDAC/tubulin inhibitors capable of exerting anti-tumor activity via mitochondrial dysfunction and apoptosis induction [70], arundinin was able to impair in vitro breast cancer cell growth, promoting the accumulation of mitochondrial ROS and apoptosis, which was confirmed by the activation of Caspase 3 and PARP, the upregulation of BAX, a relevant effector of mitochondrial apoptosis, and the downregulation of anti-apoptotic BCL2 protein. This evidence concerns the gene BCL2 and neoplasm.