JUN and non-small cell lung carcinoma: Since the EML4‐ALK in ALK+ NSCLC cells has an ALK kinase domain fragment identical to that in NPM‐ALK [38], the EML4‐ALK is thought to be similarly responsible for AP‐1 transcriptional activity, suggesting that decreased AP‐1 activity resulting from ALK‐TKI treatment in ALK+ NSCLC cells would lead to downregulation of various antioxidant gene expressions and enhancement of cellular ROS levels.