In addition to IL-6, STAT-3 can be activated by another receptor and non-receptor tyrosine kinases, such as epidermal growth factor receptor (EGFR), whose overexpression in pancreatic tumorigenesis has been implicated in neoplastic precursors and additionally, after tumor initiation, in the maintenance of MAPK/ERK activity [73,74]. Here, EGFR is linked to neoplasm.