This includes an evaluation of pro-inflammatory and immune regulatory function in macrophages and KCs, phagocytosis and chemokine activity in neutrophils, and cytotoxicity in T cells, etc. We identified NK cell exhaustion in the WD patients, with upregulation of KLRC1 and TIGIT and downregulation of CD16, TNF, IFNG, GZMB, GNLY, and CCL4. The gene discussed is CCL4; the disease is Wilson disease.