A previous study demonstrated that three well‐established ER stress inducers, including brefeldin A (BFA), tunicamycin (TM), and thapsigargin (TG), promote the ubiquitination and degradation of SLC1A5/38A2 in breast cancer cells.[44] However, it has been reported that TM induces the expression of SLC1A5/38A2 in pancreatic β‐cells.[45] Another study by Wang and colleagues[46] demonstrated that secoemestrin C induces ER stress and promotes ERAD‐mediated YAP degradation in pancreatic adenocarcinoma. Here, SLC1A5 is linked to breast cancer.