Further transcriptional analysis revealed that expression of proinflammatory cytokines, including Tnf and Il1b, which are known NF-κB activators that upregulate adhesion molecules33, was comparable between T-ALL cells and healthy T cells in the thymus and spleen (Supplementary Fig. 4c), suggesting T-ALL-mediated activation of NF-κB signaling in tumor-associated myeloid cells is not a likely mechanism for upregulation of adhesion molecules. Here, NFKB1 is linked to neoplasm.