Similar to the effect of the endogenously produced ROS in the activation of IRE1α-XBP1 in tDCs [7], we found that pharmacological scavenging of ROS prevented the induction of CHOP in tumor-associated myeloid cells [77], suggesting the common role of ROS in the induction of UPR in cancer-infiltrating myeloid cells. This evidence concerns the gene DDIT3 and neoplasm.