About 4% of patients with non-small cell lung carcinoma have a chromosomal rearrangement that generates a fusion gene between EML4 ('echinoderm microtubule-associated protein-like 4') and ALK ('anaplastic lymphoma kinase'), which results in constitutive kinase activity that contributes to carcinogenesis and seems to drive the malignant phenotype.
He is also the first researcher who (in June 2010) successfully treated a patient affected by ALK+ lymphoma with an ALK inhibitor (crizotinib).