Furthermore, it supports the emerging notion that upon ER stress, ER luminal proteins can exit the ER and gain new function as blockers of tumor suppressors, as exemplified by cell surface GRP78 forming a complex with CD109 and blocks TGF-β signaling (18), and cytosolic AGR2 as inhibitor of p53 (5), thus providing a selective advantage to tumor cells. This evidence concerns the gene TP53 and neoplasm.