It is often constitutively activated in cancer cells through different molecular mechanisms, such as mutations (EGFR) and amplification (human epidermal growth factor receptor 2, HER2) of RTKs, mutations in downstream molecules such as phosphatidylinositol-4, 5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) or AKT, or loss of function of the tumor suppressor molecule phosphatase and tensin homolog (PTEN)8. Here, ERBB2 is linked to cancer.