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. Here, FCGR3A is linked to Wilson disease.