In summation, our investigative foray illuminates the intricate role of G-CSF in advancing hepatocellular carcinoma progression, explicating a comprehensive mechanistic schema wherein G-CSF potentiates macrophage polarization towards a tumor-friendly M2 phenotype, instigates gene expression conducive to angiogenesis, and engages pivotal intracellular pathways that bolster the tenuous bridge between cancer proliferation and vascular development. Here, CSF3 is linked to neoplasm.