Kinase inhibitors can prevent the growth of cells possessing this mutation.203,208 Point mutations in CSF3R T618I and CSF3R N610 hyperactivate CSF3R, resulting in cytokine-independent growth of leukemia cells.208 The above studies revealed the critical function of N-glycosylation in maintaining the normal function of CSF3R, and provide a basis for conducting studies on the regulation of glycans in receptors. The gene discussed is CSF3R; the disease is leukemia.