Canonical NF-κB signaling, triggered by pathways such as TLR2/4-MyD88 and TNFR/TNFR2, enhances MDSC immunosuppression by increasing IL-10 and TGF-β production, thereby dampening T-cell responses and fostering tumor progression [301–303]. The gene discussed is NFKB1; the disease is neoplasm.