reported that high-mobility group box-1 (HMGB-1) in exosomes derived from lung cancer cells activated the NF-κB pathway in macrophages via toll-like receptor 2 (TLR2); this activation promoted glycolysis, which led to lactate accumulation, and ultimately promoted upregulation of PD-L1 expression and induced an immunosuppressive phenotype in the macrophages (78). This evidence concerns the gene NFKB1 and lung carcinoma.