This suggests that GSK-J4 may regulate the expression of TNF-α downstream inflammatory factors, including CCL2 and CXCL10, by inhibiting the activity of JMJD3 and increasing the level of H3K27me3 in their promoters, which may decrease the interaction between thyroid cells and inflammatory cells and slow down the occurrence and development of HT. The gene discussed is CCL2; the disease is hematocrit.