used a pancreatic epithelial cell‐specific PDX1 promoter to delete SNAIL1 or TWIST1 in a KPC (KrasLSL.G12D/+; p53R172H/+; Pdx1‐Cre) genetic engineered mouse model of pancreatic ductal adenocarcinoma and found that deletion of SNAIL1 or TWIST1 did not lead to any significant difference in metastatic potential and the number of CTCs, but rather an increased sensitivity to gemcitabine treatment (Zheng et al., 2015). The gene discussed is SNAI1; the disease is pancreatic ductal adenocarcinoma.