Pancreatic cancer with activating mutations in KRAS or BRAF occur frequently, and oncogenic pathways like RAS/RAF/MEK/ERK, the PI3K-AKT-mTOR, and TGFβ signaling converge on the activation of GLI1, promoting cellular proliferation, tumor progression, chemotherapeutic resistance, and early metastasis (142, 143). Here, KRAS is linked to pancreatic neoplasm.