Consistent with E2-ERα activation of the anticipatory UPR, T47D breast cancer cells modified with CRISPR-Cas9 to replace wild-type ERα with the constitutively active mutations ERαY537S (TYS cells) and ERαD538G (TDG cells) upregulate the UPR in the absence of estrogen (13). This evidence concerns the gene ERAS and breast cancer.