In this work, we show that GR acts as a transcriptional activator of PD-L1 and a transcriptional repressor of the major histocompatibility complex class I (MHC-I) in pancreatic cancer cells, and that GR depletion or inhibition promotes the infiltration and activity of cytotoxic T cells, leading to enhanced immune surveillance and sensitization of pancreatic tumors to immune checkpoint inhibitors. This evidence concerns the gene NR3C1 and familial pancreatic carcinoma.