In endometrial cancer cells where NR4A1 is silenced or treated with an NR4A1 antagonist, the major source of reactive oxygen species (ROS) is associated with the downregulation of TXNDC5 and IDH1 and this is supported by a significant increase in ROS and oxidative/ER stress after the silencing of TXNDC5 [55] (Table 3). This evidence concerns the gene NR4A1 and endometrial cancer.