Our data 1) supports the role of ERα‐p53 crosstalk in endocrine resistance of ERα‐positive tumors, 2) provides insight into the mechanism underlying favorable response of tumors expressing wt p53 to TAM therapy, and 3) has implications toward stratifying ERα‐positive BC patients to those who will or will not be responsive to TAM therapy. The gene discussed is TP53; the disease is breast cancer.