The elevated expression of the MAPK signature, characterizing IBC, is reflected by the high percentage of EGFR and/or ErbB2 overexpressing IBC tumours, which potentially leads to the frequent ER independency of IBC, as well as to an increased activation of NF-κB, accounting for the inverse interaction between NF-κB and ER activation. The gene discussed is EGFR; the disease is neoplasm.