BIBR1532 impacts on cell survival also through the down-regulation of Survivin in leukemia cells, although through unknown mechanisms (37, 38); our results suggest that Survivin cooperated in inducing apoptosis in SCCF1 and SCCF2 but not in SCCF3, where Caspase 3 cleavage and subsequent apoptosis at 100 μM might instead be due to the activation of alternative cell death mechanisms triggered by telomerase deprivation, such as the extrinsic pathway (48). Here, CASP3 is linked to leukemia.