The mechanisms underlying the therapeutic effect is not completely understood but there is a general consensus that it results from the co-influence of multiple actions like i) inhibiting the ligand-independent HER2/HER3 heterodimerization, ii) preventing the proteolytic cleavage of the HER2 extracellular domain and consequently the formation of the constitutively active p95HER2 fragment and iii) inducing the ADCC toward HER2-positive tumours [25, 26, 33, 36–38]. Here, ERBB3 is linked to neoplasm.