Recent studies have suggested that tumor chemoresistance involved numerous pathways and molecular mechanisms, including oncogenes (such as EGFR, PI3K/AKT, Erk, and NF-κB), tumor suppressor genes (such as p53), drug transporter pumps, mitochondrial alterations, DNA damage and repair, autophagy, epithelial-mesenchymal transition, cancer stemness, and exosomes [2]. This evidence concerns the gene TP53 and cancer.