Indeed, some of the top-ranking targets, such as HSP [34] and HDAC, have been shown to promote cell survival and tumour progression through the induction of chronic inflammation and suppression of immune cell activity in pancreatic cancer, indicating that these pathways are required for the survival of PDAC cells and evasion of T cell surveillance [6,7]. This evidence concerns the gene HSP90B2P and familial pancreatic carcinoma.