Here, using MCF-7 cells engineered to stably overexpress HRG as an experimental model of estrogen-independent cancer cell growth and endocrine resistance, we evaluated the autocrine capacity of HRG-driven HER2/HER3 signaling to stimulate FASN expression as part of the endocrine resistance program that is activated in certain subgroups of ER+ breast carcinomas. The gene discussed is ESR1; the disease is breast carcinoma.