Execution of the cell-death programme requires the activation of a family of cysteine proteases known as caspases. Specific cellular proteins are cleaved by caspases during apoptosis, including the retinoblastoma tumour-suppressor protein (RB1). A caspase-resistant RB1 can attenuate the death response to tumour necrosis factor alpha. The cleavage of RB1 during cell death, together with the increased cell death during embryonic development of Rb-knockout mice, suggests that RB1 degradation contributes to the activation of the cell-death pathway.