When Co2+ reacted with the high concentration of endogenous H2S at tumour sites, the expression of TNF-α, IL-6, and other inflammatory factors was down-regulated, which inhibited the activation of NF-κB, regulated the relative abundance of M1 and M2 macrophages, and improved the immunosuppressed tumour microenvironment. This evidence concerns the gene NFKB1 and neoplasm.