Therefore, tumor cells can avoid phagocytosis by (1) disrupting the ER stress pathway via reduced eIF2α phosphorylation, (2) secreting mutated forms of CRT (which saturate CD91 receptors on DCs), (3) trapping CRT in the mitochondria in high Stanniocalcin 1 tumors or (4) altering CRT binding sites on the cell surface (asialoglycans) [6,72,73,74,75,76]. The gene discussed is CALR; the disease is neoplasm.