To elucidate whether RARγ signaling can genuinely be a therapeutic target for PDAC, we need to validate the tumor-suppressive effects of blocking RARγ signaling and clarify the association between RARγ signaling and the TME, including CAF function and immune cell composition, by analyzing not only cancer cells but also the tumor stroma using genetically engineered mouse models or patient-derived tumor xenograft models. This evidence concerns the gene RARG and neoplasm.