Epigenetic alterations have also shown to play a role in resistance, allowing for tumor cells to rely on constitutive activation of parallel signaling pathways involving MET proto-oncogene receptor tyrosine kinase (MET), Human Epidermal growth factor Receptor 3 (HER3) and fibroblast growth factor receptor (FGFR) to bypass HER2 inhibition [98,99]. This evidence concerns the gene ERBB2 and neoplasm.