The observation that ectopic PR expression is sufficient to drive tumor growth and even metastasis when ER signaling is genetically or pharmacologically abrogated in MCF7 cells points to the possibility that this may also apply in the context of endocrine resistance, in particular in tumors with ESR1 mutations, which as a result of overactivated ER signaling show high PR expression levels. The gene discussed is ESR1; the disease is neoplasm.