The IRE1α‐XBP1S pathway has been reported to enhance or suppress cancer progression in different contexts.30, 31 On the other hand, ATF6α‐dependent UPR has shown cytoprotective functions leading to oncogenic roles in tumourigenesis.32, 33 We found that ATL treatment markedly increased XBP1S expression (Figure S2C), but decreased ATF6 expression in MDA‐MB‐231 cells (Figure S2D) indicating that ER stress and a UPR response are indeed activated after treatment with ATL. Here, ATF6 is linked to cancer.