EGFR and neoplasm: By interfering with the tyrosine kinase activity of mutated or overexpressed oncogenes, such as Epidermal Growth Factor Receptor (EGFR) or Human Epidermal Growth Factor Receptor 2 (HER2), or by simultaneously blocking multiple signaling pathways that are relevant to cancer (or to cancer angiogenesis), these drugs target biological functions that cancer cells are critically reliant on, ultimately causing cancer cell death and tumor shrinkage [1].