Although chronic inflammation can promote initial carcinogenesis by the production of several inflammatory cytokines, including IFN-γ, TNF-α, interleukin-6 (IL-6), and IL-1, in combination with the production of reactive oxygen or nitrogen species by activated myeloid cells65–67, the same pro-inflammatory cytokines released by immune cells in an ICD milieu can favor immune activation rather than suppression in the tumor microenvironment, and enable ultimately the immune system to act effectively against metastatic tumors67–69. This evidence concerns the gene IL6 and neoplasm.