Next, we targeted the Δ40p53-induced phenotype by targeting a serine/threonine-protein kinase, MELK, which is associated with DOX resistance [42], Sox2 upregulation [43], and TP53-mutant breast cancers [44] and was shown to be upregulated in Δ40p53 cells following DOX treatment [20]. This evidence concerns the gene TP53 and breast carcinoma.