In that study, MSI2 was identified as a metastatic driver that supported the protein expression of the TGFβ receptor TGFBR1, and TGFβ effector SMAD3, suggesting MSI2 was required for EMT; however, MSI2 depletion reduced CDH1 expression in NSCLC cell cultures, indicating a role in supporting epithelial identity [9]. This evidence concerns the gene TGFBR1 and non-small cell lung carcinoma.