We demonstrated that tumor-derived MDSCs activated the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/nuclear factor kappa B (NF-κB) signaling pathway in B cells through the PD-1/PD-L1 axis, which affected the immunosuppressive functions of PD-1+PD-L1+ B cells (evaluated by T cell proliferation and interferon (IFN)-γ secretion). This evidence concerns the gene NFKB1 and neoplasm.