Preclinical work in AI-resistant BC models has shown that AR activity collaborates with residual ERα signaling to sustain tumor growth despite aromatase blockade.43 Along with evidence of intratumoral androgen accumulation after exemestane therapy,44 these data support a model in which some ER-positive tumors transition from ER to AR dependence, thereby acquiring resistance to AIs. This evidence concerns the gene ESR1 and breast cancer.