The process of carcinogenesis starts in the proinflammatory microenvironment and is abided by Darwinian evolution theory: mutation-selection-adaption; and the genetic basis of this process is the generation and accumulation of somatic mutations. Currently the molecular mechanisms of massive nucleotide alterations and natural selection of mutant cells under environment pressure still remain unclear. The apolioprotein B mRNA-editing enzyme catalytic polypeptide (APOBEC) family of cytidine deaminases, which is transcriptionally induced by proinflammatory cytokine and chemokine, plays important roles in the innate and adaptive immunities of human organism. APOBECs can not only inhibit viral replication but also facilitate the generation of cancer-promoting viral mutants; they can also facilitate the generation of driver mutations in the host genes, thus contribute to the development of cancers. APOBECs, as hallmark enzymes bridging inflammation and cancer, play an important role in cancer evolution.