Furthermore, this study also found that exosomes from HT patients cocultured with DCs bind to TLR2/3 of DCs, and activate DCs through the TLR2/myeloid differentiation factor 88 (MyD88)/NF-κB and TLR3/TRIF/NF-κB pathways, thus leading to an imbalance in the differentiation of CD4+ T lymphocytes. The gene discussed is NFKB1; the disease is hematocrit.