Programmed cell death, or apoptosis, is a natural process that helps maintain the health of tissues by eliminating damaged or unnecessary cells. When this process is disrupted, cells that should die instead continue to multiply, increasing the risk of developing cancer. In France, cancer remains the leading cause of death, accounting for nearly a quarter of all deaths in 2023, with lung, colon and rectum, prostate, and pancreatic cancers among the most lethal. Cancer development, or carcinogenesis, is a complex process involving several stages. It begins with initiation, where genetic mutations in key genes—such as oncogenes or tumor suppressor genes—alter the normal function of cells, often due to exposure to harmful substances or radiation. Next, during promotion, these mutated cells multiply under the influence of environmental or hormonal signals, leading to the growth of abnormal cell clusters. Finally, in progression, further genetic changes occur, giving the cancer cells abilities such as invading surrounding tissues, evading the immune system, and spreading to other parts of the body through metastasis. A hallmark of cancer is resistance to apoptosis. Research by scientists Douglas Hanahan and Robert Weinberg shows that most, if not all, cancers develop this resistance, allowing cells with harmful genetic changes to survive and continue dividing. This resistance increases genomic instability, leading to more mutations and the growth of more aggressive cancer cells. It also plays a role in making cancer cells more adaptable, or plastic, allowing them to change their properties and become more invasive. Cancer cells can also resist apoptosis by undergoing a transformation known as the epithelial-mesenchymal transition (EMT), which makes them more mobile and less responsive to signals that would cause them to die. These cells become more tolerant to harsh conditions in the body, such as oxidative stress, allowing them to survive in challenging environments. Tumors also manipulate their surroundings by stimulating the growth of new blood vessels (angiogenesis) and releasing substances that promote inflammation, creating a favorable environment for their growth and spread. In recent years, treatments that aim to restore apoptosis have transformed cancer care. Immune checkpoint inhibitors, such as anti-PD-1 antibodies, help re-activate the immune system by blocking signals that cancer cells use to avoid detection. These therapies have improved outcomes for patients with previously difficult-to-treat cancers. However, cancer's ability to adapt complicates treatment. When cancer cells develop resistance to apoptosis, conventional therapies like chemotherapy or radiotherapy may become ineffective. Some survival pathways, such as PI3K/AKT and NF-κB, are often overactive in cancer cells, helping them survive despite treatment. This ability to evade death highlights cancer not just as a disease of uncontrolled growth, but also as a disease of "non-death," with the potential to ultimately lead to the death of the patient.