Since the release of the NKG2D ligand MICA/B could represent a tumor evasion mechanism resulting in the downregulation of NKG2D with an ensuing impaired NK cell function [25,29], we tested the hypothesis that decreased NKG2D expression on PB NK in patients could be associated with an increased soluble form of MICA/B (sMICA/B). Here, KLRK1 is linked to neoplasm.