Further, as shown in preclinical and clinical settings, compared with wtHER2, d16HER2 homodimers couple to several downstream oncogenic signal transduction pathways that increase the activation of Focal Adhesion Kinase (FAK), Phosphatidylinositol-3-Kinase/Protein Kinase B (PI3K/AKT), Mitogen-Activated Protein Kinase (MAPK) and Proto-oncogene tyrosine-protein kinase SRC (SRC), all of which have been implicated in tumor proliferation, migration, and induction of the EMT program [24,25,37,38]. This evidence concerns the gene SRC and neoplasm.