ECM structure alterations that depend on UPR activity have been pinpointed to affect other malignant tumors, among others chronic myeloid leukemia cells that maintain phosphorylated eIF2α status constitutively elevated to induce the expression of MMPs and cathepsins, being afterwards recruited within the TME to substantiate ECM remodeling and communication between tumor cells and cancer-associated fibroblasts (CAFs) (Figure 5) [204]. The gene discussed is CTSS; the disease is cancer.