CSF1 and neoplasm: Intermittent hypoxia activates the NF-κB/HIF-1α pathway, increasing pro-inflammatory mediators like COX-2, CCL2, CXCL1, PGE2, and CSF1, these mediators recruit monocytes and neutrophils to the tumor microenvironment (TME), differentiating into TAMs and Tumor-Associated Neutrophils (TAN) (107–110).