Drug-inducible senescence: friend or foe? In response to DNA-damaging agents, cancer cells can rapidly undergo apoptosis or may enter premature senescence as a potential back-up mechanism. Whether cells re-enter the cycle or execute apoptosis out of drug-mediated senescence remains unclear. A terminal arrest of the entire cancer cell population, possibly augmented through increased immunogenicity of senescent cells, is beneficial for the host. In contrast, feeder-like growth that reflects paracrine activity of senescent cells on their non-senescent neighbors, or escape from senescence based on acquired or preexisting mutations, is considered a detrimental outcome.