Excessive EGFR activation and dysfunctional signaling by TGF-β receptor (TβR)-dependent pathways, as observed in PDAC, generates multiple aberrant autocrine and paracrine interactions between the cancer cells and the tumor microenvironment that contribute to tumor desmoplasia and that may intersect with one or another of the dozen signaling cascades that are implicated in the majority of PDACs [5], [11]. This evidence concerns the gene EGFR and cancer.