Clusterin, a chaperone protein upexpressed in prostate cancer, stabilizes Ku70/BAX complexes, sequestering BAX from its ability to induce mitochondrial release of cytochrome c, thus avoiding subsequent apoptosis and promoting resistance to cisplatin; the secreted clusterin form is expressed in aggressive late stage tumours, and although its high expression may be considered an adaptive response to OS, it enhances the survival potential of cancerous cells [195]. This evidence concerns the gene BAX and neoplasm.