Apoptosis
The cell's built-in self-destruct programme, which tidily dismantles a damaged or unwanted cell without alarming its neighbours. Cancer cells disable it, and many drugs try to switch it back on.
Apoptosis is triggered from inside (DNA damage sensed by p53, which tips the balance of BCL-2 family proteins and releases enzymes called caspases) or from outside (death signals from immune cells). Tumours resist it by mutating TP53, overexpressing BCL-2 or MCL-1, or losing the proteins that would push them over the edge; 'resisting cell death' is one of the hallmarks of cancer. Chemotherapy and radiation work largely by inflicting enough damage to trigger apoptosis, venetoclax removes the BCL-2 shield directly, and the calm, non-inflammatory nature of apoptosis is why it does not, by itself, alert the immune system, unlike immunogenic cell death.