The blockade of tunicamycin-induced XBP1 splicing in pancreatic cancer cells by these compounds reduced proliferation and the colony-forming ability, arrested the cell cycle at G1 or G2/M phases, enhanced the expression of apoptotic proteins, decreased the mitochondrial membrane potential, and potentiated the anti-tumor activity of bortezomib in mice with pancreatic cancer xenograft [227]. The gene discussed is XBP1; the disease is familial pancreatic carcinoma.