Growing evidences have demonstrated the involvement of CAFs and ECMs in PDAC tumor cells epithelial-mesenchymal transition (EMT),42 as it has been suggested that CAFs drove EMT in PDAC by secreting various cytokines such as TGF-β, IL-6.42,43 In addition to providing a hypoxic environment, ECM molecules also mediate signaling from tumor cells to engage EMT pathways.23,42 Additionally, another target gene ITGB3 (integrin beta 3), a cell surface receptor facilitating cell-EMC interaction, was primarily expressed in the Tumor cells 3 population. Here, TGFB1 is linked to neoplasm.