Therefore, we propose that in response to gemcitabine stress, pancreatic cancer cells first up-regulate HAb18G/CD147 expression and then activate EGFR-STAT3 signaling via phosphorylation at tyrosine 705 to promote the transcription of STAT3 target genes, such as MMP and cyclin D1/survivin, and ultimately to increase cell survival and invasion (Figure 5F). This evidence concerns the gene EGFR and familial pancreatic carcinoma.