Notably, it was shown that Twist1 exhibited a dual role in CAFs and cancer cells in the EMT process: on the one hand, Twist1 promoted the expression and secretion of CXCL12 from CAFs, and its knockdown in CAFs inhibited tumor growth; on the other hand, activated CXCL12/CXCR4 signaling promoted EMT process through ERK/AKT-Twist1-MMP1/E-cadherin pathway in esophageal cancer cells.173. This evidence concerns the gene AKT1 and neoplasm.