Several earlier studies have reported that the targeting of mortalin-p53 interaction by natural and chemical compounds causes nuclear translocation of p53 and reactivation of its transcriptional activation function leading to growth arrest in cancer cells (Wadhwa et al., 1998; Wadhwa et al., 2000; Wadhwa et al., 2002b; Kaul et al., 2005; Widodo et al., 2007a; Lu et al., 2011; Lu et al., 2011; Grover et al., 2012; Nigam et al., 2015). This evidence concerns the gene TP53 and cancer.