Using human breast cancer cell lines, Li et al. found that CIP2A (cancerous inhibitor of PP2A) depletion significantly induced caspase-3 activation, followed by anti-PARP cleavage in two TNBC cell lines, suggesting that PP2A can induce caspase-dependent apoptosis in TNBC cells [26]. Here, CASP3 is linked to breast carcinoma.