Validation that a blockade of apoptosis due to the sustained overexpression of BCL-2 was a required step during MYC-driven tumourigenesis was shown in a mouse model of lymphoblastic leukaemia where removal of this BCL-2 reliance using an inducible system led to leukaemia remission and prolonged survival of the mice [208]. Here, BCL2 is linked to acute lymphoblastic leukemia.