Fucoidan, such as FPS1M (Laminaria japonica Areschoug) and LF2, has been shown to activate the toll-like receptor 4 (TLR4) pathway, leading to the transformation of tumor-associated macrophages from the pro-tumor M2 phenotype to the antitumor M1 phenotype, and upregulating pro-inflammatory factors (iNOS, TNF-α, IL-6, and IL-12) by PI3K/AKT/mTOR or NF-κB pathways, alleviating the immunosuppressive tumor microenvironment (Deng et al., 2024; Deng et al., 2022). The gene discussed is NFKB1; the disease is neoplasm.