Acute and temporary inflammation may inhibit tumor growth by upregulating inflammatory mediators, such as interleukins IL-1β, IL-6, IL-8, TNFα, IFNγ, and HMGB1 as pro-inflammatory cytokines, and IL-1Ra, IL-10, and IL-13 as anti-inflammatory cytokines that are part of the initial inflammatory cascade and recruit other downstream targets to enhance antitumor responses. This evidence concerns the gene IFNG and neoplasm.