Given the key function of p53 in normal stem cell self-renewal and the hypothesis that cancer is a disease of excessive self-renewal, p53 mutations in CSCs could cause excessive self-renewal.The loss of p53 led to an increase in symmetric self-renewing divisions, which resulted in the proliferation of pre-malignant mammary stem cells, and when p53 was restored, the CSC pool was reduced due to the restoration of ACDs [69]. The gene discussed is TP53; the disease is cancer.