When NKG2A/CD94 binds to its ligand such as MHC-I and HLA-E (the ligand of NKG2A in humans), such kind of interaction reduces the effector anti-tumor activity of both NK cells and T cells via recruiting SHP-1 tyrosine phosphatase in the intercellular domain of NKG2A. The gene discussed is KLRC1; the disease is neoplasm.