Studies have demonstrated that the most active and most potent tumor-enhancing effect is achieved through the HER2/HER3 dimer, which functions mostly through the downstream activation of PI3K/AKT, MAPK/ERK and JAK/STAT pathways and is responsible for treatment failure and increased resistance to therapies in breast cancer patients [53,54,55]. The gene discussed is ERBB2; the disease is breast cancer.