Assessments of other HER2-expressing tumours suggest other plausible mechanisms implied in HER2-targeting agent resistance: an inactive target receptor (such as HER2 C-terminal fragments—p95HER2 being resistant to trastuzumab) [79]; activation of target downstream components in other pathways, such as PI3K/Akt/mTOR and Ras-Raf-MAPK [80]; overexpression of other HER ligands or receptors [81]; and driver signalling from other receptors (such as the insulin-like growth factor-1 receptor (IGF1R)) [82]. This evidence concerns the gene ERBB2 and neoplasm.