In summary, our data demonstrate that inhibitory CD158ab/KIR2DL-1,-2/3 are preferentially expressed on glioblastoma-derived NK-cells and that KIR blockade is a promising tool to enhance NK-cell activity against GBM, but additional activating signals must be delivered to break functional hypoactivity of NK-cells present within the tumor. Here, KIR2DL1 is linked to neoplasm.