Similar to EREG, drugs that interfere with AREG, particularly in chemoresistant breast cancers, effectively acquiesce tumor growth, tumor-associated macrophage (TAM) infiltration [91] and block the activation of diverse EGF receptors (ErbB1, 3 and 4+ ErbB2 HER2/Neu) [92,93,94,95]. Here, ERBB2 is linked to neoplasm.