The characteristic chronic mild inflammatory condition in diabetes mellitus releases pro-inflammatory factors such as IL-6 and TNF-α through Nuclear Factor Kappa B (NF-κB)-dependent pathways, which not only directly stimulate the invasive phenotype of malignant cells but also recruit M2 macrophages and Tregs, thereby establishing an immunosuppressive microenvironment that diminishes the anti-tumor action of CD8+ T cells (131). Here, NFKB1 is linked to neoplasm.