BCL2 and breast cancer: XBP1s was reported to play a pro‐survival role and reduce the responsiveness to tamoxifen and fulvestrant through multiple mechanisms.[17, 35] For instance, ectopic expression of XBP1s protects cells from antiestrogen‐induced apoptosis by upregulation of BCL2 and mitochondrial apoptotic pathways.[36] XBP1s activates p65/RelA transcription, leading to the induction of NF‐κB, which functions as a driver for resistance to tamoxifen and fulvestrant.[13] Consistent with previous reports, we confirmed that XBP1s reduced the therapeutic response of fulvestrant in HR+/HER2− breast cancer.