Even though HER2 over-expression is considered a hallmark of aggressive breast cancer subtypes, increasing evidence has pointed toward a major contribution of Δ16HER2 splice variant (lacking exon-16), which is commonly co-expressed with wild-type HER2, in promoting cancer progression, metastasis and resistance to Trastuzumab [14, 15]. Here, ERBB2 is linked to breast carcinoma.