In light of the availability of EGFR inhibitors currently approved by the Food and Drug Administration (FDA) for the treatment of several carcinomas, namely, head and neck squamous cell carcinomas (HNSCC), nonsmall cell lung cancer (NSCLC) with specific EGFR mutations, advanced pancreatic cancer, and metastatic colorectal carcinomas without activating KRAS/BRAF mutations [27], we questioned whether EGFR‐mediated STAT3 activation could underlie PCa aggressiveness in a specific ETS molecular subtype, opening a therapeutic window for EGFR and/or STAT3 inhibitors. The gene discussed is EGFR; the disease is familial pancreatic carcinoma.