These results drive to the following assumptions: i) U3 has more potent activity than T and P in suppressing dimer formation in HER-2 positive breast cancer cells; ii) HRG addition does not seem to correlate with U3 dimerization-inhibiting activity in HER-2 positive breast cancer cells and might not represent a valuable predictive biomarker of its activity; iii) in HER-2 positive breast cancer cells, at least in vitro, HRG might act as HER-1-activating ligand and U3 seems to inhibit this activity. The gene discussed is EGFR; the disease is breast cancer.