Mutations and the overexpression of the tyrosine kinase ErbB (erythroblastic leukemia viral oncogene homolog) receptor family members (EGFR/ErbB1/HER1, ErbB2/HER2, ErbB3/HER3 and ErbB4/HER4) have been shown to play a prominent role in oncogenesis; in particular, the epidermal growth factor receptor (EGFR) and ErbB2, also denoted as human EGFR-2 (HER2), contribute to the enhanced proliferative capacity, promotion of cell survival, development of tumor-associated angiogenesis and increased migratory and invasive capacities of tumor cells. This evidence concerns the gene ERBB3 and neoplasm.