At least three strategies to disrupt the cytoplasmic sequestrated mortalin-p53 interaction, including (a) a cytoplasmically localized p53 polypeptide containing the C-terminal residues 323–337 as a competitor of p53 in the p53-mortalin interaction [34], (b) a cationic rhodacyanine dye analog MKT-077 bound to mortalin [35], and (c) shRNA-mediated mortalin silencing [33], were shown to release p53 from mortalin–p53 complexes, to mediate the nuclear translocation and reactivation of tumor-suppressive p53, and to cause growth arrest and apoptosis in different human liver cancer cells (Fig. 5). This evidence concerns the gene TP53 and neoplasm.