In addition, in human pancreatic cancer cells that overexpress NR4A1, treatment with antagonists or inactivators of nuclear NR4A1, such as 1,1-bis(3′-indolyl)-1-(p-hydroxyphenyl)methane (DIM-C-pPhOH) and fanchinoline (FCN) inhibited cell growth and induced apoptosis, and this was accompanied by the downregulation of Sp1-dependent anti-apoptotic genes and induction of ROS-mediated ER stress [2,3,7]. This evidence concerns the gene NR4A1 and pancreatic neoplasm.