Other mechanisms include stimulation of alternative pathways either by activation of other kinases, including hepatocyte growth factor receptor (MET) and human epidermal growth factor receptor 2, or alterations of key components in the EGFR pathway, including activation of phosphatidylinositol-4,5-bisphosphate 3-kinase or loss of phosphatase and tensin homolog (PTEN), which eliminate the requirement for EGFR-mediated tumor cell activation (9–14). The gene discussed is MET; the disease is neoplasm.