UPR leads cancer cells to thrive and spread through a cell-autonomous mechanism: for example, by upregulating enzymes and molecular chaperones involved in protein folding, i.e., Endoplasmic Reticulum Oxidoreductin 1 A (ERO1A), and through a cell non-autonomous mechanism regulating Vascular Endothelial Growth Factor (VEGF), the related angiogenesis, and tumor microenvironment [3–6]. This evidence concerns the gene ERO1A and neoplasm.