The evolution of CC starts with an inflammatory process that activates different signals, such as the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and hypoxia-inducible factor (HIF-1α) with a signal transducer and activator of transcription 3 (Stat3) in tumor cells which cause the production of IL-10 or transforming growth factor beta (TGF-β) in the TME by TAMs [23,24]. The gene discussed is HIF1A; the disease is neoplasm.