Both DYRK1A and DYRK3 were found to activate the nicotinamide adenosine dinucleotide (NAD)-dependent deacetylase that inactivates TP53 under stressful conditions [38], because MSI has a higher mutational load and cellular stress, DYRK1A and 3 might be required to overcome cellular stress by activating SIRT1 and enhance the survival of cancer cells [38]. This evidence concerns the gene SIRT1 and cancer.