Many in vitro studies have demonstrated that the EMT process is regulated at the transcriptional level, i.e., through silencing of CDH1. By employing a lineage-labeled LSL-KrasG12D/+; Trp53fl/+; Pdx1-Cre (KPC) mouse model (LSL-KrasG12D; P53loxP/+; Pdx1-cre; LSL-Rosa26YFP/YFP) of pancreatic ductal adenocarcinoma (PDAC) to study EMT in vivo, Aiello et al. [57] found that loss of the epithelial phenotype in many tumors was accomplished through protein internalization, resulting in a partial EMT. Here, PDX1 is linked to pancreatic ductal adenocarcinoma.