Indeed, our data reveal that co-incident with the induction of HO-1 upon adipocyte exposure, there is a significant escalation in the levels of ER chaperone BIP as well as increases in spliced XBP1, a finding indicating activation of UPR and linking oxidative stress and ER stress pathways in a context of adipocyte-driven tumor promotion. This evidence concerns the gene HMOX1 and neoplasm.