Through immunofluorescence localization, we found that CCDC25, a transmembrane protein expressed in HUVECs, was transferred to the cytoplasm after NET stimulation, activated the AKT/mTOR axis to mediate signal transduction, and promoted HUVEC proliferation, migration, and tubule formation, thereby initiating neovascularization, improving the ischemic condition of the tumor microenvironment, and promoting tumor growth. This evidence concerns the gene AKT1 and neoplasm.