Although these events are likely to be complex and multifactorial, interesting studies by Huang and colleagues showed that caspase activation in 4T1 breast tumors led to caspase-dependent iPLA2 cleavage PGE2-mediated tumor repopulation (a hallmark of apoptosis-inducible proliferation), and decreased tumorigenicity was observed in either caspase 3 or iPLA2 knockout cells [22]. Here, CASP3 is linked to neoplasm.