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auThOr’s vIew Natural killer (NK) cells play a key role in cancer immunosurveillance. In line with this notion, a robust cytotoxic activity in circulating NK cells has been associated with a reduced risk to develop cancer in subjects monitored over prolonged peri-ods of time.1,2 A delicate balance between inhibitory and activating signals regulates the functions of NK cells. Inhibitory sig-nals arise from the interaction between MCH class I molecules and various NK-cell receptors, including various members of the killer immunoglobulin-like receptor (KIR) family, killer cell lectin-like receptor sub-family C, member 1 (KLRC1, best known as NKG2A), leukocyte immunoglobulin-like receptor, subfamily B (with TM and ITIM domains), member 1 (LILRB1, best known as ILT-2). NK cells are also equipped with activatory receptors, includ-ing killer cell lectin-like receptor subfam-ily K, member 1 (KLRK1, best known as NKG2D), and several natural cytotoxicity receptors (i.e., NCR1, NCR2, and NCR3, best known as NKp46, NKp44, and NKp30, respectively), which are directly involved in the killing of transformed cells.2 Unlike NKp30 and NKp46, NKp44 it is not expressed by resting NK cells but only by their activated counterparts, which may partially explain the increased cytotoxicity of NK cells exposed to interleukin-2 (IL-2