TGFB1 and neoplasm: It was demonstrated that the crosstalk between MS, CAFs, and PDAC cells strongly reduced the Gemcitabine–NabPaclitaxel dependent inhibition of tumor cell viability through the activation of TGFβ-signaling, and that the selective inhibition of TGβR1 receptor by galunisertib, a specific inhibitor, restored the sensitivity to chemotherapy drugs and could be used in combination with gemcitabine to improve patient outcomes, as demonstrated in several studies [31,32].