In light of our in vitro evidence that CD44v6 represented a potential contributory factor to the aggressive phenotype of endocrine-resistant cells through its ability to modulate EGFR signaling, we explored this hypothesis further in a small exploratory series of formalin-fixed paraffin-embedded TMAs representing 140 patients with ER+ primary breast cancers receiving adjuvant tamoxifen with a 20-year follow-up and for which the EGFR status was already known (30). The gene discussed is EGFR; the disease is breast cancer.