Strong biological evidence supports the role of UACA in helping cancer cells escape Par-4 induced apoptosis by preventing trafficking of Par-4 receptor, GRP78, to the cancer cell surface21, whereas Par-4-dependent cancer cell multinucleation and cell death was shown indispensable for the anti-cancer activities of anti-HER2 agents and anthracyclines22. This evidence concerns the gene HSPA5 and cancer.