However, in cancer cells, these processes are upregulated and dysregulated, usually due to the abnormal function of oncogenes (e.g., K-RAS, c-MYC), tumor suppressor genes (e.g., p53, RB1, P16INK4A) or genes that have dual oncogenic and tumor suppressor functions (e.g., ATF3) leading to genomic instability and tumor progression [53,54]. This evidence concerns the gene TP53 and cancer.