Based on our observations and findings by others documenting caspase-3 activation in cancer cells exposed to CHK1 inhibitors33, 36, we conclude that BCL2-regulated apoptosis is elicited, as primary B cells or Burkitt lymphomas overexpressing BCL2 or pre-B ALL cells lacking BAX/BAK proved cell death resistant ex vivo, confirming mitochondrial apoptosis as a key event. The gene discussed is CASP3; the disease is Burkitt lymphoma.