The results showed that NSG1 overexpression boosted tumor weight, volume, and Ki-67 expression, while SB-431542 treatment inhibited the ability of NSG1 on tumorigenesis in vivo (Fig. 7A–D), demonstrated that NSG1/TGF-β axis is indispensable signaling for proliferation of ESCC cells. This evidence concerns the gene MKI67 and esophageal squamous cell carcinoma.