As previously demonstrated [4, 7], these findings suggest that wild-type ALK is silenced in normal lung cells because of lack of production, but when C-terminal ALK is fused to N-terminal EML4 in normal cells, the transcription of the kinase domain of ALK is activated by the constant promoter activity of EML4, and the resultant abundantly produced EML4-fused ALK leads to cancer through aberrant ALK signal transduction. Here, EML4 is linked to cancer.