These findings suggest that increased adhesion of ICN1 leukemia cells to ECs through LFA-1/ICAM-1 but not VLA-4/VCAM-1 may contribute to the endothelial UPR induction and leukemia bone marrow remodeling while PERK depletion restored niche function independently of these adhesion processes. The gene discussed is VCAM1; the disease is leukemia.