reported that deregulation of the TP53‐MYC axis in mammary tumors increased cancer stem cell content and plasticity and was a critical determinant of tumor growth and clinical aggressiveness [42], where MYC was a transcriptional target of TP53 in mammary stem cells and was activated in breast tumors as a consequence of TP53 loss, and similar findings were observed within TNBC [43, 44]. The gene discussed is TP53; the disease is neoplasm.