Several lines of evidence support a role for DOK2 in suppression of lung tumorigenesis driven by oncogenic EGFR. First, we observe loss of DOK2 in human lung adenocarcinoma and association of this feature with somatic mutation of EGFR. Second, DOK2 overexpression inhibited the tumor-forming ability of lung adenocarcinoma cells harboring an EGFR mutation. This evidence concerns the gene DOK2 and neoplasm.