KRAS and neoplasm: In the high-risk group, a variety of pathways involved in remodeling tumor microenvironment matrix and promoting tumor metastasis (such as angiogenesis, hypoxia, apical junction, epithelial mesenchymal transformation, myogenesis, etc.) and pathways closely related to tumor cell proliferation and differentiation (upregulation of KRAS signal, dysfunction of hedgehog signal, NOTCH signal and TGFβ signal, etc.) were highly enriched.