In response to tumour progression, NO and RNS stimulate the passage of immune cells from the bloodstream around cancer cells, the polarization of tumour-associated macrophages (TAMs), the transactivation of eNOS/iNOS, the stabilization of HIF1α, the transcription of proangiogenic factors, the activation of S-nitrosylation, the inactivation of Janus kinase 3, early response kinase, and protein kinase B, which prevent the IL-2 response. The gene discussed is HIF1A; the disease is neoplasm.