Based on a previous study, which reported that high-mobility group AT-hook 1 (HMGA1) promotes chemoresistance to gemcitabine through an Akt-dependent mechanism in human pancreatic cancer cells [114], Hassan et al. introduce a new strategy of delivering decoy HMGA1-hyperbinding sites into the nucleus of pancreatic cancer cells using an engineered adenovirus, leading to the sequestration of excess amounts of nuclear HMGA1 with the decoy hyperbinding sites and resulting in the reduction of oncogenic pancreatic cells and HMGA1-associated gemcitabine resistance [115]. Here, AKT1 is linked to pancreatic neoplasm.