Although these models are biologically relevant to ΔNp63α’s role in basal-like cancers, and our previous study had proved that activation of HER2 promotes tumor metastasis by suppressing ΔNp63α expression [14], the generalizability of our conclusions to luminal subtypes remains untested, where ΔNp63α expression is minimal and distinct regulatory mechanisms may dominate. The gene discussed is ERBB2; the disease is neoplasm.