The other mechanism of calreticulin-mediated regulation of EMT was revealed in pancreatic cancer cells: Calreticulin can promote EGF-induced EMT by enhancing cell migration/invasion and decreasing E-cadherin; it was due to calreticulin-conferred activation of the integrin/EGFR-ERK/MAPK signaling pathway, which includes EGFR phosphorylation at tyrosine 1173 [277]. Here, CALR is linked to familial pancreatic carcinoma.