Approximately 3–7% of nonsmall cell lung cancer (NSCLC) patients have neoplasms with constitutive anaplastic large-cell lymphoma kinase (ALK) activity due to ALK abnormalities, most frequently in the form of intrachromosomal inversion and consequent ALK rearrangement with the partner echinoderm microtubule associated protein-like 4 (EML4) forming EML4-ALK fusion. Here, EML4 is linked to neoplasm.