CSF1 (colony-stimulating factor 1) is a cytokine essential for mononuclear phagocyte survival, proliferation, and differentiation, particularly of macrophages and monocytes. It promotes pro-inflammatory chemokine release and plays critical roles in innate immunity, bone resorption regulation, and fertility 1. CSF1 signaling through its cognate receptor CSF1R regulates macrophage polarization and function, with significant implications for cancer immunology. In cancer, CSF1 functions as a key mediator of immune escape. The PKCα/ZFP64/CSF1 axis drives anti-PD1 resistance in hepatocellular carcinoma by promoting M2 macrophage polarization and creating an immunosuppressive tumor microenvironment 2. Similarly, mutant p53 upregulates CSF1 expression via BRD4-dependent mechanisms to promote epithelial-to-mesenchymal transition and metastasis in esophageal squamous cell carcinoma 3. The osteopontin-CSF1-CSF1R axis facilitates tumor-associated macrophage trafficking and expansion in HCC, with therapeutic blockade sensitizing tumors to anti-PD-L1 therapy 4. CSF1-mediated macrophage recruitment and polarization also occurs in non-malignant diseases. In IgA nephropathy, mesangial cells express elevated CSF1 levels that drive macrophage infiltration and promote glomerulonephritis progression 5. In pancreatic cancer, alternative splicing regulation of CSF1 promotes M2 macrophage polarization through the IGF2BP2/CSF1/CSF1R axis 6. Therapeutically, CSF1/CSF1R axis inhibition represents a promising immunotherapy combination strategy across multiple cancer types 7.