As the most aggressive breast tumors arise from deregulation of MaSCs homeostasis and self-renewal37, and p53 is found mutated in nearly 40% of human breast cancers28, we anticipate that experiments addressing the mechanisms underpinning the working principles of Insc in p53-KO MaSCs in vivo might be instrumental to the development of novel therapeutical strategies targeting breast cancer stem cells. The gene discussed is TP53; the disease is breast carcinoma.