As previously rationalized [2], the UBXN2A-mot-2 dependent anti-cancer mechanism of VTD combined with DNA damage mechanisms triggered by conventional chemotherapy can be considered a novel treatment strategy wherein two different but interconnected pathways can selectively choose cancer cells with high levels of mot-2 and high pools of inactivated p53 versus normal cells with low mot-2 in the cytoplasm. This evidence concerns the gene HSPA9 and cancer.