EML4–ALK proteins are highly transforming and pathogenic in NSCLC due to increased oligomerization and constitutive, kinase-activating autophosphorylation: through activation of several downstream signaling pathways such as RAS/MAP kinase and PI3K/AKT, they lead to cell proliferation and de-differentiation. The gene discussed is EML4; the disease is non-small cell lung carcinoma.