The upregulation of pro-senescence markers CDKN1A (p21) and CDKN2B (p15)—master effectors of multiple tumour suppressor pathways—and pro-apoptotic markers, such as BBC3, BAX, BID and BAK1, also contributes to the regulation of cell homeostasis, although our in vitro data of combination therapy indicate that synergy between treatments is not dependent on increased apoptosis. The gene discussed is BID; the disease is neoplasm.