Engl.; it increased the externalization of phosphatidylserine residues and the apoptotic DNA fragmentation in HeLa cervical cancer cells, activated certain caspases (–8,–9,–3) and caused the cleavage of the poly(ADP ribose) polymerase (PARP-1), induced mitochondrial membrane depolarization, increased Bax/Bcl-2 ratio and triggered endoplasmic reticulum stress (164). This evidence concerns the gene BAX and cervical cancer.