In this sense, TAMs promote tumor progression through the secretion of various cytokines (e.g., CSF-1, CCL2) and activation of a signal transducer and activator of transcription 3 (STAT-3), NF-κB, and hypoxia-inducible factor-1 (HIF-1) pathways, secreting immunosuppressive mediators and pro-angiogenic factors that facilitate immune evasion and neovascularization [109,110]. The gene discussed is HIF1A; the disease is neoplasm.