Adaptive mechanisms against the prolonged metabolic stresses in tumor microenvironment, constitutive activation of UPR, and overexpression of ER chaperone proteins like GRP78, have been studied in multiple cancer types as being linked to tumor processes such as invasion, resistance to environmental stressors, angiogenesis, oncogenic signaling, and resistance to traditional therapy [17,39]. Here, HSPA5 is linked to neoplasm.