In the microenvironment of CRC, dense infiltrate of immune cells stimulates the secretion of proinflammatory cytokines, such as interleukin- (IL-) 6, IL-8, IL-1β, and TNF-α, which can synergistically activate signal transducer and activator of transcription 3 (STAT3), nuclear factor kappa-B (NF-κB), and hypoxia-inducible factor 1α (HIF-1α) pathways, resulting in progression of CRC [44, 45]. This evidence concerns the gene HIF1A and colorectal carcinoma.