KRas depletion induced caspase-3 activation and PARP cleavage in MiaPaCa2 and L3.6pl (pancreatic), SW620 (colon), and Calu-6 (lung) cells but did not in A549 and H460 (lung) and DLD-1 and HCT-8 (colon) human cancer cells (Fig. 2a), indicating that the former four tumor cell lines are mutant KRas-dependent, whereas the latter four cell lines are not. Here, CASP3 is linked to neoplasm.