Cancer cells often acquire mutations that disrupt apoptotic pathways, allowing them to evade cell death and continue proliferating. Common mechanisms include overexpression of anti-apoptotic proteins like Bcl-2, downregulation or mutation of pro-apoptotic proteins such as Bax, and loss of function in tumor suppressor genes like p53, which plays a crucial role in inducing apoptosis in response to cellular stress. Furthermore, cancer cells may express decoy receptors or inhibitory proteins that prevent the activation of death receptors.