The epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor has demonstrated limited survival benefits for patients with pancreatic cancer due to mutated KRAS [41], however, the inactivation of PCSK6 may be a novel target of treatment, bypassing mutated KRAS and retarding tumor progression in pancreatic cancer, providing that a direct interaction between PACE4 and the Raf-MEK1/2-ERK1/2 axis can be proven in the future. This evidence concerns the gene EGFR and neoplasm.