Notably, in ERα+ breast cancer cells engineered to model antigen‐presenting features, E2 treatment attenuates IFN‐γ‐driven CIITA transcription and subsequent HLA‐DR expression, which suppression can be fully reversed by the endoplasmic reticulum (ER) antagonist or ESR1 knockdown, demonstrating direct ERα engagement at CIITA pIV58 (relevance to pancreatic APCs remains to be validated). This evidence concerns the gene ESR1 and breast cancer.