HLA-E and neoplasm: Similarly, in the setting of an infection, blocking the interaction between NK cell inhibitory receptors [e.g., CD159a (NKG2A), CD158a (KIR2DL1), and 158b (KIR2DL2)] and MHC class I molecules (e.g., HLA-C and HLA-E) on HIV-infected autologous tumor cells resulted in a drastic increase in killing of anti-gp120-coated HIV-infected cells by NK cells [154].