The latter is particularly important since the translocation of GRP78 from the ER to the cell surface is actively promoted by stress, and on the cell surface, csGRP78 assumes novel functions beyond the ER and regulates multiple oncogenic pathways, including the PI3K/AKT pathway, which is a major driver of tumor proliferation, resistance and metastasis [8, 17–23]. Here, HSPA5 is linked to neoplasm.