A recent study by Borde et al., reported that treatment in different breast cancer cell lines, including a high SigmaR1 expressing TNBC and an estrogen receptor (ER) + (low-SigmaR1 expressing) with the SigmaR1 antagonist 1-(4-iodophenyl)-3-(2-adamantyl)guanidine (IPAG) activated the UPR in both cell lines and caused aggregation and colocalization of the receptor with the ER-stress marker binding immunoglobulin protein (BiP) in the tamoxifen-resistant LY2 cells [40]. This evidence concerns the gene ESR1 and breast cancer.