Hence, above findings suggested that EGFR and its downstream Ras-MAPK pathway may activate HSF1 via induce the PTSs of pancreatic acinar cells indirectly, in other words, HSF1 may acts as the sensor of EGFR-Ras-MAPK hyper-activation induced PTSs during pancreatic cancer tumorigenesis, however, the exact mechanism has yet to be elucidated. This evidence concerns the gene HSF1 and pancreatic neoplasm.