ERBB2 and neoplasm: HER2 alterations in NSCLC include mutations (typically in the kinase domain, exons 18–21), gene amplifications leading to increased HER2 copies, and receptor overexpression identified via immunohistochemistry (IHC), which refers to an excess of HER2 receptors on tumor cell surfaces and plays a key role in selecting targeted therapies, such as trastuzumab deruxtecan (T-DXd), which directly inhibits HER2-driven cancer progression [93].