This suggests that a potential mechanism of TPA-induced transcription of VIL2 V1 is the activation of the MEK/ERK1/2 pathway, which leads to enhanced expression of Sp1, c-Fos, and c-Jun and promotion of their binding to TRE within the promoter region of VIL2 V1, ultimately resulting in the up-regulation of VIL2 V1 in ESCC cells. This evidence concerns the gene JUN and esophageal squamous cell carcinoma.