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. The gene discussed is EGFR; the disease is pancreatic neoplasm.