Reactive nitrogen species (RNS) form a multidimensional regulatory network in the tumor microenvironment (TME) through three core mechanisms: autonomous generation by tumor cells (via hypoxia/HIF-1α and inflammation/NF-κB-driven iNOS upregulation) and immune cells (e.g., TAMs and TANs via TLR-mediated iNOS activation), intracellular modulation of key tumor cell functions (proliferation, apoptosis, invasion, and metabolic reprogramming), and intercellular signaling interactions with immune, stromal, and vascular components. This evidence concerns the gene HIF1A and neoplasm.