LCC9 cells are more dependent on BCL2 for their survival, since they exhibit a significantly greater growth inhibition by the small molecule BCL2 inhibitor HA 14-1 when compared with their LCC1 controls, and the LCC9 antiestrogen-resistant cells also express lower IRF1, indicating that a clear functional link exists between IRF1, NF-κB activation, BCL2 expression, and ER+ breast cancer cell fate [62, 68]. This evidence concerns the gene ESR1 and breast carcinoma.