Tumor-derived immunosuppressive factors like β-catenin activation, PGE2, GCSF, impaired intra-tumoral cDC1 chemokine production like CCL4, CCL5, CXCL12, or defects in cDC1 precursor differentiation in the bone marrow mediating intra-tumoral cDC1 dysfunction should also be further explored and validated (9, 19, 21, 23). This evidence concerns the gene CSF3 and neoplasm.