Host microenvironment factors, such as the bioavailability of EGF and IGF‐1 at indolent tumour sites, have been shown to modulate plasticity of certain breast tumours.39, 40 Thus, we interrogated RTK activity to further explain why NF‐κB inhibition stimulated significant HMEC proliferation. The gene discussed is NFKB1; the disease is neoplasm.