The primary objective of this study is to elucidate the mechanism by which the reagent UCN-01 induces apoptosis when administered to leukemia cells along with HmG-CoA reductase inhibitors, mainly the statins. In this study, we demonstrated that exposure of leukemia cell lines to lovastatin (20 uM, 18 hours) and UCN-01 (100 nM, 18 hours) resulted in mitochondria dysfunction, procaspase 3 and 9 cleavage, and PAW degradation along with marked cytochrome C release and apoptosis. Although similar molecular mechanisms have not yet been confirmed in other cancers, our hypothesis holds that enhanced apoptotic effects of UCN-01 are due in part to lovastatin's ability to block formation of geranylgeranylpyrophosphate and farnesylpyrophosphate by interfering with the rate-limiting step of the mevalonate pathway. Geranylgeranylpyrophosphate and farnesylpyrophosphate induce post-translational modifications in RAS that anchor the protein to the cell membrane so that it acts as a signal transducer to the nucleus, promoting cell proliferation.