CASP3 and cancer: Exposure of cancer cells or normal human fibroblasts to the transcriptional inhibitor actinomycin D (ActD) resulted in increases in the percentage of AnnexinV+ cells and activate caspase-3 and caused proteolytic cleavage of inactive pro-caspase-3 and PARP form into activated cleaving enzymes, whereas this process was suppressed by the caspase-3 inhibitor Ac-DEVD-CMK (Figure 1D–F).