Besides, we also found EGFR and its downstream MEK/mTOR closely participated the active-phosphorylation and nuclear-translocation of HSF1 in pancreatic acinar cells; interestingly, the EGFR-Ras-MAPK pathway may activate HSF1 via induce the PTSs of pancreatic acinar cells indirectly, in other words, the abnormal level of HSF1 during pancreatic cancer tumorigenesis may be a passive response of the cells against to the increasing PTSs. This evidence concerns the gene MTOR and pancreatic neoplasm.