They upregulated NF-kB p65 by reducing the PI3Kγ protein in macrophages and tumor cells, which efficiently polarized macrophages toward proinflammatory macrophages and activated the immune response by increasing the population of CD8+ and CD4+ T cells, B cells, NK cells and Treg cells, collectively inhibiting tumor growth and reshaping the immunosuppressive TME [154]. This evidence concerns the gene NFKB1 and neoplasm.