Altogether, these data strongly support the case that bortezomib can augment the strength of activation signals in antigen-specific CD8+T cells in the tumor microenvironment via cytokine receptors and downstream PI3K/Akt/NFκB/STAT5 pathways, which together sustain the differentiation of CD8+T cells into terminal effectors. The gene discussed is NFKB1; the disease is neoplasm.