In view of the earlier reports describing differential subcellular distribution of mortalin in normal and cancer cells [8, 10, 11], we screened a library of 12,000 small molecules for their ability to disrupt mortalin-p53 interactions leading to (i) shift in mortalin staining from perinuclear (typical of cancer cells) to pancytoplasmic (typical of normal cells) and (ii) nuclear translocation of p53 (Additional file 1: Figure S1A). This evidence concerns the gene TP53 and cancer.