Conversely, HPV<sup>-</sup> tumors upregulated CLEC2C and CLEC2D ligands on tumor cell surfaces, engaging the inhibitory receptor KLRB1 on NK cells; this CLEC2-KLRB1 axis correlated with suppressed NK activity and poorer prognosis, and was confirmed at the protein level by IHC. This evidence concerns the gene CLEC1B and neoplasm.